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  • Articles  (722)
  • Elsevier  (722)
  • American Chemical Society
  • American Chemical Society (ACS)
  • Springer Science + Business Media
  • Neuron  (722)
  • 315
  • Medicine  (722)
  • 1
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    Neural Correlates of Reinforcement Learning in Mid-lateral Cerebellum (2020)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 27 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Naveen Sendhilnathan, Anna E. Ipata, Michael E. Goldberg〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉The role of the cerebellum in non-motor learning is poorly understood. Here, we investigated the activity of Purkinje cells (P-cells) in the mid-lateral cerebellum as the monkey learned to associate one arbitrary symbol with the movement of the left hand and another with the movement of the right hand. During learning, but not when the monkey had learned the association, the simple spike responses of P-cells reported the outcome of the animal’s most recent decision without concomitant changes in other sensorimotor parameters such as hand movement, licking, or eye movement. At the population level, P-cells collectively maintained a memory of the most recent decision throughout the entire trial. As the monkeys learned the association, the magnitude of this reward-related error signal approached zero. Our results provide a major departure from the current understanding of cerebellar processing and have critical implications for cerebellum’s role in cognitive control.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627319310980-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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  • 2
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    Human Herpesvirus 6 Detection in Alzheimer’s Disease Cases and Controls across Multiple Cohorts (2020)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 23 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Mary Alice Allnutt, Kory Johnson, David A. Bennett, Sarah M. Connor, Juan C. Troncoso, Olga Pletnikova, Marilyn S. Albert, Susan M. Resnick, Sonja W. Scholz, Philip L. De Jager, Steven Jacobson〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉The interplay between viral infection and Alzheimer’s disease (AD) has long been an area of interest, but proving causality has been elusive. Several recent studies have renewed the debate concerning the role of herpesviruses, and human herpesvirus 6 (HHV-6) in particular, in AD. We screened for HHV-6 detection across three independent AD brain repositories using (1) RNA sequencing (RNA-seq) datasets and (2) DNA samples extracted from AD and non-AD control brains. The RNA-seq data were screened for pathogens against taxon references from over 25,000 microbes, including 118 human viruses, whereas DNA samples were probed for PCR reactivity to HHV-6A and HHV-6B. HHV-6 demonstrated little specificity to AD brains over controls by either method, whereas other viruses, such as Epstein-Barr virus (EBV) and cytomegalovirus (CMV), were detected at comparable levels. These direct methods of viral detection do not suggest an association between HHV-6 and AD.〈/p〉〈/div〉
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  • 3
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    Multiple Rhythm-Generating Circuits Act in Tandem with Pacemaker Properties to Control the Start and Speed of Locomotion (2020)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 22 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Jianren Song, Irene Pallucchi, Jessica Ausborn, Konstantinos Ampatzis, Maria Bertuzzi, Pierre Fontanel, Laurence D. Picton, Abdeljabbar El Manira〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉In vertebrates, specific command centers in the brain can selectively drive slow-explorative or fast-speed locomotion. However, it remains unclear how the locomotor central pattern generator (CPG) processes descending drive into coordinated locomotion. Here, we reveal, in adult zebrafish, a logic of the V2a interneuron rhythm-generating circuits involving recurrent and hierarchical connectivity that acts in tandem with pacemaker properties to provide an ignition and gear-shift mechanism to start locomotion and change speed. A comprehensive mapping of synaptic connections reveals three recurrent circuit modules engaged sequentially to increase locomotor speed. The connectivity between V2a interneurons of different modules displayed a clear asymmetry in favor of connections from faster to slower modules. The interplay between V2a interneuron pacemaker properties and their organized connectivity provides a mechanism for locomotor initiation and speed control. Thus, our results provide mechanistic insights into how the spinal CPG transforms descending drive into locomotion and align its speed with the initial intention.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627319310967-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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  • 4
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    Thomas Blanpied (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: 22 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 105, Issue 2〈/p〉 〈p〉Author(s): 〈/p〉 〈div〉〈p〉In an interview with 〈em〉Neuron〈/em〉, Dr. Thomas Blanpied talks about why he became a neuroscientist, what inspires him to investigate protein organization at synapses, politicization being one of the biggest challenges for science, and why passion is important for driving science forward.〈/p〉〈/div〉
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  • 5
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    Communication, Cross Talk, and Signal Integration in the Adult Hippocampal Neurogenic Niche (2020)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2020
    Description: 〈p〉Publication date: 22 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 105, Issue 2〈/p〉 〈p〉Author(s): Cinzia Vicidomini, Nannan Guo, Amar Sahay〈/p〉 〈div〉〈p〉Radial glia-like neural stem cells (RGLs) in the dentate gyrus subregion of the hippocampus give rise to dentate granule cells (DGCs) and astrocytes throughout life, a process referred to as adult hippocampal neurogenesis. Adult hippocampal neurogenesis is sensitive to experiences, suggesting that it may represent an adaptive mechanism by which hippocampal circuitry is modified in response to environmental demands. Experiential information is conveyed to RGLs, progenitors, and adult-born DGCs via the neurogenic niche that is composed of diverse cell types, extracellular matrix, and afferents. Understanding how the niche performs its functions may guide strategies to maintain its health span and provide a permissive milieu for neurogenesis. Here, we first discuss representative contributions of niche cell types to regulation of neural stem cell (NSC) homeostasis and maturation of adult-born DGCs. We then consider mechanisms by which the activity of multiple niche cell types may be coordinated to communicate signals to NSCs. Finally, we speculate how NSCs integrate niche-derived signals to govern their regulation.〈/p〉〈/div〉
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  • 6
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    LRRTM4: A Novel Regulator of Presynaptic Inhibition and Ribbon Synapse Arrangements of Retinal Bipolar Cells (2020)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 20 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Raunak Sinha, Tabrez J. Siddiqui, Nirmala Padmanabhan, Julie Wallin, Chi Zhang, Benyamin Karimi, Fred Rieke, Ann Marie Craig, Rachel O. Wong, Mrinalini Hoon〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉LRRTM4 is a transsynaptic adhesion protein regulating glutamatergic synapse assembly on dendrites of central neurons. In the mouse retina, we find that LRRTM4 is enriched at GABAergic synapses on axon terminals of rod bipolar cells (RBCs). Knockout of LRRTM4 reduces RBC axonal GABA〈sub〉A〈/sub〉 and GABA〈sub〉C〈/sub〉 receptor clustering and disrupts presynaptic inhibition onto RBC terminals. LRRTM4 removal also perturbs the stereotyped output synapse arrangement at RBC terminals. Synaptic ribbons are normally apposed to two distinct postsynaptic “dyad” partners, but in the absence of LRRTM4, “monad” and “triad” arrangements are also formed. RBCs from retinas deficient in GABA release also demonstrate dyad mis-arrangements but maintain LRRTM4 expression, suggesting that defects in dyad organization in the LRRTM4 knockout could originate from reduced GABA receptor function. LRRTM4 is thus a key synapse organizing molecule at RBC terminals, where it regulates function of GABAergic synapses and assembly of RBC synaptic dyads.〈/p〉〈/div〉
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  • 7
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    Estimation of Current and Future Physiological States in Insular Cortex (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 16 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Yoav Livneh, Arthur U. Sugden, Joseph C. Madara, Rachel A. Essner, Vanessa I. Flores, Lauren A. Sugden, Jon M. Resch, Bradford B. Lowell, Mark L. Andermann〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Interoception, the sense of internal bodily signals, is essential for physiological homeostasis, cognition, and emotions. While human insular cortex (InsCtx) is implicated in interoception, the cellular and circuit mechanisms remain unclear. We imaged mouse InsCtx neurons during two physiological deficiency states: hunger and thirst. InsCtx ongoing activity patterns reliably tracked the gradual return to homeostasis but not changes in behavior. Accordingly, while artificial induction of hunger or thirst in sated mice via activation of specific hypothalamic neurons (AgRP or SFO〈sup〉GLUT〈/sup〉) restored cue-evoked food- or water-seeking, InsCtx ongoing activity continued to reflect physiological satiety. During natural hunger or thirst, food or water cues rapidly and transiently shifted InsCtx population activity to the future satiety-related pattern. During artificial hunger or thirst, food or water cues further shifted activity 〈em〉beyond〈/em〉 the current satiety-related pattern. Together with circuit-mapping experiments, these findings suggest that InsCtx integrates visceral-sensory signals of current physiological state with hypothalamus-gated amygdala inputs that signal upcoming ingestion of food or water to compute a prediction of future physiological state.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627319310931-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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  • 8
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    Opposing Contributions of GABAergic and Glutamatergic Ventral Pallidal Neurons to Motivational Behaviors (2020)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 13 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Marcus Stephenson-Jones, Christian Bravo-Rivera, Sandra Ahrens, Alessandro Furlan, Xiong Xiao, Carolina Fernandes-Henriques, Bo Li〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉The ventral pallidum (VP) is critical for invigorating reward seeking and is also involved in punishment avoidance, but how it contributes to such opposing behavioral actions remains unclear. Here, we show that GABAergic and glutamatergic VP neurons selectively control behavior in opposing motivational contexts. 〈em〉In vivo〈/em〉 recording combined with optogenetics in mice revealed that these two populations oppositely encode positive and negative motivational value, are differentially modulated by animal’s internal state, and determine the behavioral response during motivational conflict. Furthermore, GABAergic VP neurons are essential for movements toward reward in a positive motivational context but suppress movements in an aversive context. In contrast, glutamatergic VP neurons are essential for movements to avoid a threat but suppress movements in an appetitive context. Our results indicate that GABAergic and glutamatergic VP neurons encode the drive for approach and avoidance, respectively, with the balance between their activities determining the type of motivational behavior.〈/p〉〈/div〉
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  • 9
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    Amygdala Reward Neurons Form and Store Fear Extinction Memory (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 14 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Xiangyu Zhang, Joshua Kim, Susumu Tonegawa〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉The ability to extinguish conditioned fear memory is critical for adaptive control of fear response, and its impairment is a hallmark of emotional disorders like post-traumatic stress disorder (PTSD). Fear extinction is thought to take place when animals form a new memory that suppresses the original fear memory. However, little is known about the nature and the site of formation and storage of this new extinction memory. Here we demonstrate that a fear extinction memory engram is formed and stored in a genetically distinct basolateral amygdala (BLA) neuronal population that drives reward behaviors and antagonizes the BLA’s original fear neurons. Activation of fear extinction engram neurons and natural reward-responsive neurons overlap significantly in the BLA. Furthermore, these two neuronal subsets are mutually interchangeable in driving reward behaviors and fear extinction behaviors. Thus, fear extinction memory is a newly formed reward memory.〈/p〉〈/div〉
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  • 10
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    Endocannabinoid Signaling Collapse Mediates Stress-Induced Amygdalo-Cortical Strengthening (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 13 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): David J. Marcus, Gaurav Bedse, Andrew D. Gaulden, James D. Ryan, Veronika Kondev, Nathan D. Winters, Luis E. Rosas-Vidal, Megan Altemus, Ken Mackie, Francis S. Lee, Eric Delpire, Sachin Patel〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Functional coupling between the amygdala and the dorsomedial prefrontal cortex (dmPFC) has been implicated in the generation of negative affective states; however, the mechanisms by which stress increases amygdala-dmPFC synaptic strength and generates anxiety-like behaviors are not well understood. Here, we show that the mouse basolateral amygdala (BLA)-prelimbic prefrontal cortex (plPFC) circuit is engaged by stress and activation of this pathway in anxiogenic. Furthermore, we demonstrate that acute stress exposure leads to a lasting increase in synaptic strength within a reciprocal BLA-plPFC-BLA subcircuit. Importantly, we identify 2-arachidonoylglycerol (2-AG)-mediated endocannabinoid signaling as a key mechanism limiting glutamate release at BLA-plPFC synapses and the functional collapse of multimodal 2-AG signaling as a molecular mechanism leading to persistent circuit-specific synaptic strengthening and anxiety-like behaviors after stress exposure. These data suggest that circuit-specific impairment in 2-AG signaling could facilitate functional coupling between the BLA and plPFC and the translation of environmental stress to affective pathology.〈/p〉〈/div〉
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    Dopamine-Evoked Synaptic Regulation in the Nucleus Accumbens Requires Astrocyte Activity (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 15 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Michelle Corkrum, Ana Covelo, Justin Lines, Luigi Bellocchio, Marc Pisansky, Kelvin Loke, Ruth Quintana, Patrick E. Rothwell, Rafael Lujan, Giovanni Marsicano, Eduardo D. Martin, Mark J. Thomas, Paulo Kofuji, Alfonso Araque〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Dopamine is involved in physiological processes like learning and memory, motor control and reward, and pathological conditions such as Parkinson’s disease and addiction. In contrast to the extensive studies on neurons, astrocyte involvement in dopaminergic signaling remains largely unknown. Using transgenic mice, optogenetics, and pharmacogenetics, we studied the role of astrocytes on the dopaminergic system. We show that in freely behaving mice, astrocytes in the nucleus accumbens (NAc), a key reward center in the brain, respond with Ca〈sup〉2+〈/sup〉 elevations to synaptically released dopamine, a phenomenon enhanced by amphetamine. In brain slices, synaptically released dopamine increases astrocyte Ca〈sup〉2+〈/sup〉, stimulates ATP/adenosine release, and depresses excitatory synaptic transmission through activation of presynaptic A〈sub〉1〈/sub〉 receptors. Amphetamine depresses neurotransmission through stimulation of astrocytes and the consequent A〈sub〉1〈/sub〉 receptor activation. Furthermore, astrocytes modulate the acute behavioral psychomotor effects of amphetamine. Therefore, astrocytes mediate the dopamine- and amphetamine-induced synaptic regulation, revealing a novel cellular pathway in the brain reward system.〈/p〉〈/div〉
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  • 12
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    Astrocyte Unfolded Protein Response Induces a Specific Reactivity State that Causes Non-Cell-Autonomous Neuronal Degeneration (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 7 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Heather L. Smith, Oliver J. Freeman, Adrian J. Butcher, Staffan Holmqvist, Ibrahim Humoud, Tobias Schätzl, Daniel T. Hughes, Nicholas C. Verity, Dean P. Swinden, Joseph Hayes, Lis de Weerd, David H. Rowitch, Robin J.M. Franklin, Giovanna R. Mallucci〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Recent interest in astrocyte activation states has raised the fundamental question of how these cells, normally essential for synapse and neuronal maintenance, become pathogenic. Here, we show that activation of the unfolded protein response (UPR), specifically phosphorylated protein kinase R-like endoplasmic reticulum (ER) kinase (PERK-P) signaling—a pathway that is widely dysregulated in neurodegenerative diseases—generates a distinct reactivity state in astrocytes that alters the astrocytic secretome, leading to loss of synaptogenic function 〈em〉in vitro〈/em〉. Further, we establish that the same PERK-P-dependent astrocyte reactivity state is harmful to neurons 〈em〉in vivo〈/em〉 in mice with prion neurodegeneration. Critically, targeting this signaling exclusively in astrocytes during prion disease is alone sufficient to prevent neuronal loss and significantly prolongs survival. Thus, the astrocyte reactivity state resulting from UPR over-activation is a distinct pathogenic mechanism that can by itself be effectively targeted for neuroprotection.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627319310566-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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  • 13
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    TREM2 Regulates Microglial Cholesterol Metabolism upon Chronic Phagocytic Challenge (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 2 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Alicia A. Nugent, Karin Lin, Bettina van Lengerich, Steve Lianoglou, Laralynne Przybyla, Sonnet S. Davis, Ceyda Llapashtica, Junhua Wang, Do Jin Kim, Dan Xia, Anthony Lucas, Sulochanadevi Baskaran, Patrick C.G. Haddick, Melina Lenser, Timothy K. Earr, Ju Shi, Jason C. Dugas, Benjamin J. Andreone, Todd Logan, Hilda O. Solanoy〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Loss-of-function (LOF) variants of TREM2, an immune receptor expressed in microglia, increase Alzheimer’s disease risk. TREM2 senses lipids and mediates myelin phagocytosis, but its role in microglial lipid metabolism is unknown. Combining chronic demyelination paradigms and cell sorting with RNA sequencing and lipidomics, we find that wild-type microglia acquire a disease-associated transcriptional state, while TREM2-deficient microglia remain largely homeostatic, leading to neuronal damage. TREM2-deficient microglia phagocytose myelin debris but fail to clear myelin cholesterol, resulting in cholesteryl ester (CE) accumulation. CE increase is also observed in APOE-deficient glial cells, reflecting impaired brain cholesterol transport. This finding replicates in myelin-treated TREM2-deficient murine macrophages and human iPSC-derived microglia, where it is rescued by an ACAT1 inhibitor and LXR agonist. Our studies identify TREM2 as a key transcriptional regulator of cholesterol transport and metabolism under conditions of chronic myelin phagocytic activity, as TREM2 LOF causes pathogenic lipid accumulation in microglia.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627319310499-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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  • 14
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    Cortical Synaptic AMPA Receptor Plasticity during Motor Learning (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 31 December 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Richard H. Roth, Robert H. Cudmore, Han L. Tan, Ingie Hong, Yong Zhang, Richard L. Huganir〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Modulation of synaptic strength through trafficking of AMPA receptors (AMPARs) is a fundamental mechanism underlying synaptic plasticity, learning, and memory. However, the dynamics of AMPAR trafficking 〈em〉in vivo〈/em〉 and its correlation with learning have not been resolved. Here, we used 〈em〉in vivo〈/em〉 two-photon microscopy to visualize surface AMPARs in mouse cortex during the acquisition of a forelimb reaching task. Daily training leads to an increase in AMPAR levels at a subset of spatially clustered dendritic spines in the motor cortex. Surprisingly, we also observed increases in spine AMPAR levels in the visual cortex. There, synaptic potentiation depends on the availability of visual input during motor training, and optogenetic inhibition of visual cortex activity impairs task performance. These results indicate that motor learning induces widespread cortical synaptic potentiation by increasing the net trafficking of AMPARs into spines, including in non-motor brain regions.〈/p〉〈/div〉
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  • 15
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    Pathogenic Variants in CEP85L Cause Sporadic and Familial Posterior Predominant Lissencephaly (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 24 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Meng-Han Tsai, Alison M. Muir, Won-Jing Wang, Yi-Ning Kang, Kun-Chuan Yang, Nian-Hsin Chao, Mei-Feng Wu, Ying-Chao Chang, Brenda E. Porter, Laura A. Jansen, Guillaume Sebire, Nicolas Deconinck, Wen-Lang Fan, Shih-Chi Su, Wen-Hung Chung, Edith P. Almanza Fuerte, Michele G. Mehaffey, University of Washington Center for Mendelian Genomics, Ching-Ching Ng, Chung-Kin Chan, Kheng-Seang Lim〈/p〉
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  • 16
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    Posterior Neocortex-Specific Regulation of Neuronal Migration by CEP85L Identifies Maternal Centriole-Dependent Activation of CDK5 (2020)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 24 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Andrew Kodani, Connor Kenny, Abbe Lai, Dilenny M. Gonzalez, Edward Stronge, Gabrielle M. Sejourne, Laura Isacco, Jennifer N. Partlow, Anne O’Donnell, Kirsty McWalter, Alicia B. Byrne, A. James Barkovich, Edward Yang, R. Sean Hill, Pawel Gawlinski, Wojciech Wiszniewski, Julie S. Cohen, S. Ali Fatemi, Kristin W. Baranano, Mustafa Sahin〈/p〉
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    Science that Inspires (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: 19 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 105, Issue 4〈/p〉 〈p〉Author(s): The Cell Press Team〈/p〉
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    Dopaminergic Transmission Rapidly and Persistently Enhances Excitability of D1 Receptor-Expressing Striatal Projection Neurons (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 18 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Asha K. Lahiri, Mark D. Bevan〈/p〉
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    Causal Role of Motor Preparation during Error-Driven Learning (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 12 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Saurabh Vyas, Daniel J. O’Shea, Stephen I. Ryu, Krishna V. Shenoy〈/p〉
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    Inference-Based Decisions in a Hidden State Foraging Task: Differential Contributions of Prefrontal Cortical Areas (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 11 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Pietro Vertechi, Eran Lottem, Dario Sarra, Beatriz Godinho, Isaac Treves, Tiago Quendera, Matthijs Nicolai Oude Lohuis, Zachary F. Mainen〈/p〉
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    Parietal Cortex Regulates Visual Salience and Salience-Driven Behavior (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 10 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Xiaomo Chen, Marc Zirnsak, Gabriel M. Vega, Eshan Govil, Stephen G. Lomber, Tirin Moore〈/p〉
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    Replay of Behavioral Sequences in the Medial Prefrontal Cortex during Rule Switching (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 6 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Karola Kaefer, Michele Nardin, Karel Blahna, Jozsef Csicsvari〈/p〉
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    Direct Fit to Nature: An Evolutionary Perspective on Biological and Artificial Neural Networks (2020)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2020
    Description: 〈p〉Publication date: 5 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 105, Issue 3〈/p〉 〈p〉Author(s): Uri Hasson, Samuel A. Nastase, Ariel Goldstein〈/p〉
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    Richard H. Masland (1942–2019) (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: 5 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 105, Issue 3〈/p〉 〈p〉Author(s): Peter Sterling, Heinz Wässle, Thomas Euler〈/p〉
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    A Role for the Locus Coeruleus in Hippocampal CA1 Place Cell Reorganization during Spatial Reward Learning (2020)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 21 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Alexandra Mansell Kaufman, Tristan Geiller, Attila Losonczy〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉During spatial learning, hippocampal (HPC) place maps reorganize to represent new goal locations, but little is known about the circuit mechanisms facilitating these changes. Here, we examined how neuromodulation via locus coeruleus (LC) projections to HPC area CA1 (LC-CA1) regulates the overrepresentation of CA1 place cells near rewarded locations. Using two-photon calcium imaging, we monitored the activity of LC-CA1 fibers in the mouse dorsal HPC. We find that the LC-CA1 projection signals the translocation of a reward, predicting behavioral performance on a goal-oriented spatial learning task. An optogenetic stimulation mimicking this LC-CA1 activity induces place cell reorganization around a familiar reward, while its inhibition decreases the degree of overrepresentation around a translocated reward. Our results show that LC acts in conjunction with other factors to induce goal-directed reorganization of HPC representations and provide a better understanding of the role of neuromodulatory actions on HPC place map plasticity.〈/p〉〈/div〉
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    Functional Electron Microscopy (“Flash and Freeze”) of Identified Cortical Synapses in Acute Brain Slices (2020)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 9 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Carolina Borges-Merjane, Olena Kim, Peter Jonas〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉How structural and functional properties of synapses relate to each other is a fundamental question in neuroscience. Electrophysiology has elucidated mechanisms of synaptic transmission, and electron microscopy (EM) has provided insight into morphological properties of synapses. Here we describe an enhanced method for functional EM (“flash and freeze”), combining optogenetic stimulation with high-pressure freezing. We demonstrate that the improved method can be applied to intact networks in acute brain slices and organotypic slice cultures from mice. As a proof of concept, we probed vesicle pool changes during synaptic transmission at the hippocampal mossy fiber-CA3 pyramidal neuron synapse. Our findings show overlap of the docked vesicle pool and the functionally defined readily releasable pool and provide evidence of fast endocytosis at this synapse. Functional EM with acute slices and slice cultures has the potential to reveal the structural and functional mechanisms of transmission in intact, genetically perturbed, and disease-affected synapses.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627319310888-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    A Neuroethics Framework for the Australian Brain Initiative (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: 8 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 105, Issue 1〈/p〉 〈p〉Author(s): Australian Brain Alliance〈/p〉
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    Editorial Note to: Consolidation Promotes the Emergence of Representational Overlap in the Hippocampus and Medial Prefrontal Cortex (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: 8 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 105, Issue 1〈/p〉 〈p〉Author(s): Alexa Tompary, Lila Davachi〈/p〉
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    Consolidation Promotes the Emergence of Representational Overlap in the Hippocampus and Medial Prefrontal Cortex (2020)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2020
    Description: 〈p〉Publication date: 8 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 105, Issue 1〈/p〉 〈p〉Author(s): Alexa Tompary, Lila Davachi〈/p〉
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    Turning Touch into Perception (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: 8 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 105, Issue 1〈/p〉 〈p〉Author(s): Ranulfo Romo, Román Rossi-Pool〈/p〉 〈div〉〈p〉Many brain areas modulate their activity during vibrotactile tasks. The activity from these areas may code the stimulus parameters, stimulus perception, or perceptual reports. Here, we discuss findings obtained in behaving monkeys aimed to understand these processes. In brief, neurons from the somatosensory thalamus and primary somatosensory cortex (S1) only code the stimulus parameters during the stimulation periods. In contrast, areas downstream of S1 code the stimulus parameters during not only the task components but also perception. Surprisingly, the midbrain dopamine system is an actor not considered before in perception. We discuss the evidence that it codes the subjective magnitude of a sensory percept. The findings reviewed here may help us to understand where and how sensation transforms into perception in the brain.〈/p〉〈/div〉
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    Deep Multilayer Brain Proteomics Identifies Molecular Networks in Alzheimer’s Disease Progression (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 8 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Bing Bai, Xusheng Wang, Yuxin Li, Ping-Chung Chen, Kaiwen Yu, Kaushik Kumar Dey, Jay M. Yarbro, Xian Han, Brianna M. Lutz, Shuquan Rao, Yun Jiao, Jeffrey M. Sifford, Jonghee Han, Minghui Wang, Haiyan Tan, Timothy I. Shaw, Ji-Hoon Cho, Suiping Zhou, Hong Wang, Mingming Niu〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Alzheimer’s disease (AD) displays a long asymptomatic stage before dementia. We characterize AD stage-associated molecular networks by profiling 14,513 proteins and 34,173 phosphosites in the human brain with mass spectrometry, highlighting 173 protein changes in 17 pathways. The altered proteins are validated in two independent cohorts, showing partial RNA dependency. Comparisons of brain tissue and cerebrospinal fluid proteomes reveal biomarker candidates. Combining with 5xFAD mouse analysis, we determine 15 Aβ-correlated proteins (e.g., MDK, NTN1, SMOC1, SLIT2, and HTRA1). 5xFAD shows a proteomic signature similar to symptomatic AD but exhibits activation of autophagy and interferon response and lacks human-specific deleterious events, such as downregulation of neurotrophic factors and synaptic proteins. Multi-omics integration prioritizes AD-related molecules and pathways, including amyloid cascade, inflammation, complement, WNT signaling, TGF-β and BMP signaling, lipid metabolism, iron homeostasis, and membrane transport. Some Aβ-correlated proteins are colocalized with amyloid plaques. Thus, the multilayer omics approach identifies protein networks during AD progression.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S089662731931058X-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    m6A mRNA Methylation Is Essential for Oligodendrocyte Maturation and CNS Myelination (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: 22 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 105, Issue 2〈/p〉 〈p〉Author(s): Huan Xu, Yulia Dzhashiashvili, Ankeeta Shah, Rejani B. Kunjamma, Yi-lan Weng, Benayahu Elbaz, Qili Fei, Joshua S. Jones, Yang I. Li, Xiaoxi Zhuang, Guo-li Ming, Chuan He, Brian Popko〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉The molecular mechanisms that govern the maturation of oligodendrocyte lineage cells remain unclear. Emerging studies have shown that N〈sup〉6〈/sup〉-methyladenosine (m〈sup〉6〈/sup〉A), the most common internal RNA modification of mammalian mRNA, plays a critical role in various developmental processes. Here, we demonstrate that oligodendrocyte lineage progression is accompanied by dynamic changes in m〈sup〉6〈/sup〉A modification on numerous transcripts. 〈em〉In vivo〈/em〉 conditional inactivation of an essential m〈sup〉6〈/sup〉A writer component, METTL14, results in decreased oligodendrocyte numbers and CNS hypomyelination, although oligodendrocyte precursor cell (OPC) numbers are normal. 〈em〉In vitro Mettl14〈/em〉 ablation disrupts postmitotic oligodendrocyte maturation and has distinct effects on OPC and oligodendrocyte transcriptomes. Moreover, the loss of 〈em〉Mettl14〈/em〉 in oligodendrocyte lineage cells causes aberrant splicing of myriad RNA transcripts, including those that encode the essential paranodal component neurofascin 155 (NF155). Together, our findings indicate that dynamic RNA methylation plays an important regulatory role in oligodendrocyte development and CNS myelination.〈/p〉〈/div〉
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    Activity-Dependent Plasticity of Axo-axonic Synapses at the Axon Initial Segment (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 27 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Alejandro Pan-Vazquez, Winnie Wefelmeyer, Victoria Gonzalez Sabater, Guilherme Neves, Juan Burrone〈/p〉
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    Context-Dependent Decision Making in a Premotor Circuit (2020)
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 26 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Zheng Wu, Ashok Litwin-Kumar, Philip Shamash, Alexei Taylor, Richard Axel, Michael N. Shadlen〈/p〉
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    Accelerating the Evolution of Nonhuman Primate Neuroimaging (2020)
    Elsevier
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    Publication Date: 2020
    Description: 〈p〉Publication date: 19 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 105, Issue 4〈/p〉 〈p〉Author(s): The PRIMatE Data Exchange (PRIME-DE) Global Collaboration Workshop and Consortium〈/p〉
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    Advanced Neurotechnologies for the Restoration of Motor Function (2020)
    Elsevier
    In: Neuron
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    Description: 〈p〉Publication date: 19 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 105, Issue 4〈/p〉 〈p〉Author(s): Silvestro Micera, Matteo Caleo, Carmelo Chisari, Friedhelm C. Hummel, Alessandra Pedrocchi〈/p〉
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    Nucleocytoplasmic Proteomic Analysis Uncovers eRF1 and Nonsense-Mediated Decay as Modifiers of ALS/FTD C9orf72 Toxicity (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 13 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Juan A. Ortega, Elizabeth L. Daley, Sukhleen Kour, Marisa Samani, Liana Tellez, Haley S. Smith, Elizabeth A. Hall, Y. Taylan Esengul, Yung-Hsu Tsai, Tania F. Gendron, Christopher J. Donnelly, Teepu Siddique, Jeffrey N. Savas, Udai B. Pandey, Evangelos Kiskinis〈/p〉
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    Thalamus Modulates Consciousness via Layer-Specific Control of Cortex (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 12 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Michelle J. Redinbaugh, Jessica M. Phillips, Niranjan A. Kambi, Sounak Mohanta, Samantha Andryk, Gaven L. Dooley, Mohsen Afrasiabi, Aeyal Raz, Yuri B. Saalmann〈/p〉
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    Artificial and Natural Intelligence: From Invention to Discovery (2020)
    Elsevier
    In: Neuron
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    Description: 〈p〉Publication date: 5 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 105, Issue 3〈/p〉 〈p〉Author(s): Li Zhaoping〈/p〉
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    Cue-Evoked Dopamine Promotes Conditioned Responding during Learning (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 5 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Joachim Morrens, Çağatay Aydin, Aliza Janse van Rensburg, José Esquivelzeta Rabell, Sebastian Haesler〈/p〉
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    LRRTMs Organize Synapses through Differential Engagement of Neurexin and PTPσ (2020)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 28 January 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Reiko T. Roppongi, Shreya H. Dhume, Nirmala Padmanabhan, Prabhisha Silwal, Nazmeena Zahra, Benyamin Karimi, Claire Bomkamp, Chetan S. Patil, Kevin Champagne-Jorgensen, Rebecca E. Twilley, Peng Zhang, Michael F. Jackson, Tabrez J. Siddiqui〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Presynaptic neurexins (Nrxs) and type IIa receptor-type protein tyrosine phosphatases (RPTPs) organize synapses through a network of postsynaptic ligands. We show that leucine-rich-repeat transmembrane neuronal proteins (LRRTMs) differentially engage the protein domains of Nrx but require its heparan sulfate (HS) modification to induce presynaptic differentiation. Binding to the HS of Nrx is sufficient for LRRTM3 and LRRTM4 to induce synaptogenesis. We identify mammalian Nrx1γ as a potent synapse organizer and reveal LRRTM4 as its postsynaptic ligand. Mice expressing a mutant form of LRRTM4 that cannot bind to HS show structural and functional deficits at dentate gyrus excitatory synapses. Through the HS of Nrx, LRRTMs also recruit PTPσ to induce presynaptic differentiation but function to varying degrees in its absence. PTPσ forms a robust complex with Nrx, revealing an unexpected interaction between the two presynaptic hubs. These findings underscore the complex interplay of synapse organizers in specifying the molecular logic of a neural circuit.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627320300039-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    Prefrontal Cortex Corticotropin-Releasing Factor Neurons Control Behavioral Style Selection under Challenging Situations (2020)
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    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 25 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Peng Chen, Shihao Lou, Zhao-Huan Huang, Zhenni Wang, Qing-Hong Shan, Yu Wang, Yupeng Yang, Xiangning Li, Hui Gong, Yan Jin, Zhi Zhang, Jiang-Ning Zhou〈/p〉
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    Combined Phase-Rate Coding by Persistently Active Neurons as a Mechanism for Maintaining Multiple Items in Working Memory in Humans (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 20 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Jan Kamiński, Aneta Brzezicka, Adam N. Mamelak, Ueli Rutishauser〈/p〉
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    Individual Variation in Functional Topography of Association Networks in Youth (2020)
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    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 19 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Zaixu Cui, Hongming Li, Cedric H. Xia, Bart Larsen, Azeez Adebimpe, Graham L. Baum, Matt Cieslak, Raquel E. Gur, Ruben C. Gur, Tyler M. Moore, Desmond J. Oathes, Aaron F. Alexander-Bloch, Armin Raznahan, David R. Roalf, Russell T. Shinohara, Daniel H. Wolf, Christos Davatzikos, Danielle S. Bassett, Damien A. Fair, Yong Fan〈/p〉
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    Assembly-Specific Disruption of Hippocampal Replay Leads to Selective Memory Deficit (2020)
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    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 17 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Igor Gridchyn, Philipp Schoenenberger, Joseph O’Neill, Jozsef Csicsvari〈/p〉
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    Optimizing Nervous System-Specific Gene Targeting with Cre Driver Lines: Prevalence of Germline Recombination and Influencing Factors (2020)
    Elsevier
    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 5 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Lin Luo, Mateusz C. Ambrozkiewicz, Fritz Benseler, Cui Chen, Emilie Dumontier, Susanne Falkner, Elisabetta Furlanis, Andrea M. Gomez, Naosuke Hoshina, Wei-Hsiang Huang, Mary Anne Hutchison, Yu Itoh-Maruoka, Laura A. Lavery, Wei Li, Tomohiko Maruo, Junko Motohashi, Emily Ling-Lin Pai, Kenneth A. Pelkey, Ariane Pereira, Thomas Philips〈/p〉
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    A Multi-regional Network Encoding Heading and Steering Maneuvers in Drosophila (2020)
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    In: Neuron
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    Publication Date: 2020
    Description: 〈p〉Publication date: Available online 4 February 2020〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Hiroshi M. Shiozaki, Kazumi Ohta, Hokto Kazama〈/p〉
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    Bursting Enables GRP Neurons to Engage Spinal Itch Circuits (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 3 July 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 1〈/p〉 〈p〉Author(s): Hugues Petitjean, Philippe Séguéla, Reza Sharif-Naeini〈/p〉 〈div〉〈p〉In this issue of 〈em〉Neuron〈/em〉, Pagani et al. (2019) find that itch signaling occurs only when GRP neurons fire action potentials in bursts. This enables GRP release and the activation of GRPR neurons, which help carry the itch signal to the brain.〈/p〉〈/div〉
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    Exploring the Peripheral Initiation of Parkinson’s Disease in Animal Models (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 21 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 4〈/p〉 〈p〉Author(s): Zachary A. Sorrentino, Benoit I. Giasson〈/p〉 〈div〉〈p〉Parkinson’s disease is a neurodegenerative movement disorder; however, peripheral symptoms can arise decades prior. In this issue of 〈em〉Neuron〈/em〉, Kim et al. (2019) provide evidence that progressive α-synuclein aggregation initiating in the gut could be a pathogenic epicenter anatomically rippling throughout the nervous system.〈/p〉〈/div〉
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    Of Pathways, Processes, and Orbitofrontal Cortex (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 21 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 4〈/p〉 〈p〉Author(s): Vincent D. Costa〈/p〉 〈div〉〈p〉Orbitofrontal cortex (OFC) predicts the consequences of our actions and updates our expectations based on experienced outcomes. In this issue of 〈em〉Neuron〈/em〉, Groman et al. (2019) precisely ablate pathways between the OFC, amygdala, and nucleus accumbens to reveal their separable contributions to reinforcement learning.〈/p〉〈/div〉
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    Loss of NaV1.2-Dependent Backpropagating Action Potentials in Dendrites Contributes to Autism and Intellectual Disability (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 21 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 4〈/p〉 〈p〉Author(s): Leonard K. Kaczmarek〈/p〉 〈div〉〈p〉Mutations in voltage-dependent sodium channels cause severe autism/intellectual disability. In this issue of 〈em〉Neuron〈/em〉, Spratt et al. (2019) show that lowering expression of Nav1.2 channels attenuates backpropagation of action potentials into dendrites of cortical neurons, preventing spike-timing-dependent synaptic plasticity.〈/p〉〈/div〉
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    Ganglion Cells in Primate Retina Use Fuzzy Logic to Encode Complex Visual Receptive Fields (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 21 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 4〈/p〉 〈p〉Author(s): Jeffrey S. Diamond〈/p〉 〈div〉〈p〉In most neurons, all spikes look alike. However, in this issue of 〈em〉Neuron〈/em〉, Rhoades et al. (2019) describe a ganglion cell in primate retina that reports visual input to different regions of its receptive field with distinct action potential waveforms.〈/p〉〈/div〉
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    A Societal Sleep Prescription (2019)
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    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 21 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 4〈/p〉 〈p〉Author(s): Matthew P. Walker〈/p〉 〈div〉〈p〉We are suffering a global sleep-loss epidemic. The health consequences within an individual are well characterized. But does society suffer just as much? Here, I discuss how insufficient sleep erodes our societal fabric as much as it does our biological fabric, and offer some prescriptive remedies.〈/p〉〈/div〉
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    Neuromodulation of Spike-Timing-Dependent Plasticity: Past, Present, and Future (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 21 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 4〈/p〉 〈p〉Author(s): Zuzanna Brzosko, Susanna B. Mierau, Ole Paulsen〈/p〉 〈div〉〈p〉Spike-timing-dependent synaptic plasticity (STDP) is a leading cellular model for behavioral learning and memory with rich computational properties. However, the relationship between the millisecond-precision spike timing required for STDP and the much slower timescales of behavioral learning is not well understood. Neuromodulation offers an attractive mechanism to connect these different timescales, and there is now strong experimental evidence that STDP is under neuromodulatory control by acetylcholine, monoamines, and other signaling molecules. Here, we review neuromodulation of STDP, the underlying mechanisms, functional implications, and possible involvement in brain disorders.〈/p〉〈/div〉
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    Locus Coeruleus, Noradrenaline, and Behavior: Network Effect, Network Effects? (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 21 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 4〈/p〉 〈p〉Author(s): Sebastien Bouret〈/p〉 〈div〉〈p〉How does the noradrenergic nucleus locus coeruleus act on target networks to regulate behavior? In this issue of 〈em〉Neuron〈/em〉, Zerbi et al. (2019) combine functional neuroimaging and pharmacogenetics in mice to tackle that question, uncovering a network action underlying stress. And providing insight for cognition?〈/p〉〈/div〉
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    Distinct Contributions of Whisker Sensory Cortex and Tongue-Jaw Motor Cortex in a Goal-Directed Sensorimotor Transformation (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 8 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Johannes M. Mayrhofer, Sami El-Boustani, Georgios Foustoukos, Matthieu Auffret, Keita Tamura, Carl C.H. Petersen〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉The neural circuits underlying goal-directed sensorimotor transformations in the mammalian brain are incompletely understood. Here, we compared the role of primary tongue-jaw motor cortex (tjM1) and primary whisker sensory cortex (wS1) in head-restrained mice trained to lick a reward spout in response to whisker deflection. Two-photon microscopy combined with microprisms allowed imaging of neuronal network activity across cortical layers in transgenic mice expressing a genetically encoded calcium indicator. Early-phase activity in wS1 encoded the whisker sensory stimulus and was necessary for detection of whisker stimuli. Activity in tjM1 encoded licking direction during task execution and was necessary for contralateral licking. Pre-stimulus activity in tjM1, but not wS1, was predictive of lick direction and contributed causally to small preparatory jaw movements. Our data reveal a shift in coding scheme from wS1 to tjM1, consistent with the hypothesis that these areas represent cortical start and end points for this goal-directed sensorimotor transformation.〈/p〉〈/div〉
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    The Basal Ganglia Sensory System Listens to Prefrontal Task Needs (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 7 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 3〈/p〉 〈p〉Author(s): Mitsuko Watabe-Uchida〈/p〉 〈div〉〈p〉The prefrontal cortex modifies the sensory system to focus attention. In this issue of 〈em〉Neuron〈/em〉, Nakajima et al. (2019) fill the gap between the prefrontal cortex and the sensory system with an overlooked basal ganglia pathway.〈/p〉〈/div〉
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    Timing Rewarding Movements (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 7 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 3〈/p〉 〈p〉Author(s): Rachael Stentiford, Nadia L. Cerminara〈/p〉 〈div〉〈p〉Preparatory activity is found across the motor network. In this issue of 〈em〉Neuron〈/em〉, Chabrol et al. (2019) show that preparatory activity in the anterior lateral motor cortex (ALM) and cerebellum is related to the prediction of reward delivery and that the cerebellum provides a learned timing signal to the ALM.〈/p〉〈/div〉
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    Re-exploring Mechanisms of Exploration (2019)
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    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 7 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 3〈/p〉 〈p〉Author(s): Tamar Reitich-Stolero, Kristoffer C. Aberg, Rony Paz〈/p〉 〈div〉〈p〉Deciding when to exploit what is already known and when to explore new possibilities is crucial for adapting to novel and dynamic environments. Using reinforcement-based decision making, Costa et al. (2019) in this issue of 〈em〉Neuron〈/em〉 find that neurons in the amygdala and ventral-striatum differentially signal the benefit from exploring new options and exploiting familiar ones.〈/p〉〈/div〉
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    Reliable Sequential Activation of Neural Assemblies by Single Pyramidal Cells in a Three-Layered Cortex (2019)
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    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 19 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Mike Hemberger, Mark Shein-Idelson, Lorenz Pammer, Gilles Laurent〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Recent studies reveal the occasional impact of single neurons on surround firing statistics and even simple behaviors. Exploiting the advantages of a simple cortex, we examined the influence of single pyramidal neurons on surrounding cortical circuits. Brief activation of single neurons triggered reliable sequences of firing in tens of other excitatory and inhibitory cortical neurons, reflecting cascading activity through local networks, as indicated by delayed yet precisely timed polysynaptic subthreshold potentials. The evoked patterns were specific to the pyramidal cell of origin, extended over hundreds of micrometers from their source, and unfolded over up to 200 ms. Simultaneous activation of pyramidal cell pairs indicated balanced control of population activity, preventing paroxysmal amplification. Single cortical pyramidal neurons can thus trigger reliable postsynaptic activity that can propagate in a reliable fashion through cortex, generating rapidly evolving and non-random firing sequences reminiscent of those observed in mammalian hippocampus during “replay” and in avian song circuits.〈/p〉〈/div〉
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    Synergistic Coding of Visual Information in Columnar Networks (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 6 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Sunny Nigam, Sorin Pojoga, Valentin Dragoi〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Incoming stimuli are encoded collectively by populations of cortical neurons, which transmit information by using a neural code thought to be predominantly redundant. Redundant coding is widely believed to reflect a design choice whereby neurons with overlapping receptive fields sample environmental stimuli to convey similar information. Here, we performed multi-electrode laminar recordings in awake monkey V1 to report significant synergistic interactions between nearby neurons within a cortical column. These interactions are clustered non-randomly across cortical layers to form synergy and redundancy hubs. Homogeneous sub-populations comprising synergy hubs decode stimulus information significantly better compared to redundancy hubs or heterogeneous sub-populations. Mechanistically, synergistic interactions emerge from the stimulus dependence of correlated activity between neurons. Our findings suggest a refinement of the prevailing ideas regarding coding schemes in sensory cortex: columnar populations can efficiently encode information due to synergistic interactions even when receptive fields overlap and shared noise between cells is high.〈/p〉〈/div〉
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    Unlimited Genetic Switches for Cell-Type-Specific Manipulation (2019)
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    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 5 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Jorge Garcia-Marques, Ching-Po Yang, Isabel Espinosa-Medina, Kent Mok, Minoru Koyama, Tzumin Lee〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Gaining independent genetic access to discrete cell types is critical to interrogate their biological functions as well as to deliver precise gene therapy. Transcriptomics has allowed us to profile cell populations with extraordinary precision, revealing that cell types are typically defined by a unique combination of genetic markers. Given the lack of adequate tools to target cell types based on multiple markers, most cell types remain inaccessible to genetic manipulation. Here we present CaSSA, a platform to create unlimited genetic switches based on CRISPR/Cas9 (Ca) and the DNA repair mechanism known as single-strand annealing (SSA). CaSSA allows engineering of independent genetic switches, each responding to a specific gRNA. Expressing multiple gRNAs in specific patterns enables multiplex cell-type-specific manipulations and combinatorial genetic targeting. CaSSA is a new genetic tool that conceptually works as an unlimited number of recombinases and will facilitate genetic access to cell types in diverse organisms.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627319306038-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    Convergent Temperature Representations in Artificial and Biological Neural Networks (2019)
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    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 31 July 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Martin Haesemeyer, Alexander F. Schier, Florian Engert〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Discoveries in biological neural networks (BNNs) shaped artificial neural networks (ANNs) and computational parallels between ANNs and BNNs have recently been discovered. However, it is unclear to what extent discoveries in ANNs can give insight into BNN function. Here, we designed and trained an ANN to perform heat gradient navigation and found striking similarities in computation and heat representation to a known zebrafish BNN. This included shared ON- and OFF-type representations of absolute temperature and rates of change. Importantly, ANN function critically relied on zebrafish-like units. We furthermore used the accessibility of the ANN to discover a new temperature-responsive cell type in the zebrafish cerebellum. Finally, constraining the ANN by the 〈em〉C. elegans〈/em〉 motor repertoire retuned sensory representations indicating that our approach generalizes. Together, these results emphasize convergence of ANNs and BNNs on stereotypical representations and that ANNs form a powerful tool to understand their biological counterparts.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627319306014-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    Enhanced mGlu5 Signaling in Excitatory Neurons Promotes Rapid Antidepressant Effects via AMPA Receptor Activation (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 13 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Amrei Holz, Felix Mülsch, Martin K. Schwarz, Michael Hollmann, Mate D. Döbrössy, Volker A. Coenen, Marlene Bartos, Claus Normann, Knut Biber, Dietrich van Calker, Tsvetan Serchov〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Conventional antidepressants have limited efficacy and many side effects, highlighting the need for fast-acting and specific medications. Induction of the synaptic protein Homer1a mediates the effects of different antidepressant treatments, including the rapid action of ketamine and sleep deprivation (SD). We show here that mimicking Homer1a upregulation via intravenous injection of cell-membrane-permeable TAT-Homer1a elicits rapid antidepressant effects in various tests. Similar to ketamine and SD, 〈em〉in vitro〈/em〉 and 〈em〉in vivo〈/em〉 application of TAT-Homer1a enhances mGlu5 signaling, resulting in increased mTOR pathway phosphorylation, and upregulates synaptic AMPA receptor expression and activity. The antidepressant action of SD and Homer1a induction depends on mGlu5 activation specifically in excitatory CaMK2a neurons and requires enhanced AMPA receptor activity, translation, and trafficking. Moreover, our data demonstrate a pronounced therapeutic potential of different TAT-fused peptides that directly modulate mGlu5 and AMPA receptor activity and thus might provide a novel strategy for rapid and effective antidepressant treatment.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627319306373-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    ADF/Cofilin-Mediated Actin Turnover Promotes Axon Regeneration in the Adult CNS (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 7 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Andrea Tedeschi, Sebastian Dupraz, Michele Curcio, Claudia J. Laskowski, Barbara Schaffran, Kevin C. Flynn, Telma E. Santos, Sina Stern, Brett J. Hilton, Molly J.E. Larson, Christine B. Gurniak, Walter Witke, Frank Bradke〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Injured axons fail to regenerate in the adult CNS, which contrasts with their vigorous growth during embryonic development. We explored the potential of re-initiating axon extension after injury by reactivating the molecular mechanisms that drive morphogenetic transformation of neurons during development. Genetic loss- and gain-of-function experiments followed by time-lapse microscopy, 〈em〉in vivo〈/em〉 imaging, and whole-mount analysis show that axon regeneration is fueled by elevated actin turnover. Actin depolymerizing factor (ADF)/cofilin controls actin turnover to sustain axon regeneration after spinal cord injury through its actin-severing activity. This pinpoints ADF/cofilin as a key regulator of axon growth competence, irrespective of developmental stage. These findings reveal the central role of actin dynamics regulation in this process and elucidate a core mechanism underlying axon growth after CNS trauma. Thereby, neurons maintain the capacity to stimulate developmental programs during adult life, expanding their potential for plasticity. Thus, actin turnover is a key process for future regenerative interventions.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627319306336-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    CaM Kinase: Still Inspiring at 40 (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 7 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 3〈/p〉 〈p〉Author(s): K. Ulrich Bayer, Howard Schulman〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉The Ca〈sup〉2+〈/sup〉/calmodulin (CaM)-dependent protein kinase II (CaMKII) was touted as a memory molecule, even before its involvement in long-term potentiation (LTP) was shown. The enzyme has not disappointed, with subsequent demonstrations of remarkable structural and regulatory properties. Its neuronal functions now extend to long-term depression (LTD), and last year saw the first direct evidence for memory storage by CaMKII. Although CaMKII may have taken the spotlight, it is a member of a large family of diverse and interesting CaM kinases. Our aim is to place CaMKII in context of the other CaM kinases and then review certain aspects of this kinase that are of current interest.〈/p〉〈/div〉
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    The Ministry of Fear: ‘The Conjuring’ of Fright in the Amygdala by the Raphe (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 7 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 3〈/p〉 〈p〉Author(s): Praachi Tiwari, Sashaina E. Fanibunda, Vidita A. Vaidya〈/p〉 〈div〉〈p〉In this issue of 〈em〉Neuron〈/em〉, Sengupta and Holmes (2019) characterize a distinct serotonergic circuit from the dorsal raphe nucleus to the basal amygdala that facilitates fear conditioning and memory.〈/p〉〈/div〉
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    Bursting Enables GRP Neurons to Engage Spinal Itch Circuits (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 7 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 3〈/p〉 〈p〉Author(s): Hugues Petitjean, Philippe Séguéla, Reza Sharif-Naeini〈/p〉
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    Cholinergic Interneurons Provide a Link to Balance Excitation across Striatal Output Neurons (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 7 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 3〈/p〉 〈p〉Author(s): Sheng Gong, Christopher P. Ford〈/p〉 〈div〉〈p〉D1-MSNs and D2-MSNs mediate output from the accumbens. How activity of one regulates the other is poorly understood. In this issue of 〈em〉Neuron〈/em〉, Francis et al. (2019) show that D1-MSN firing induces D2-MSN LTP via the recruitment of cholinergic interneurons.〈/p〉〈/div〉
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    Ring of Power: A Band of Peptidergic Midbrain Neurons that Binds Motivation (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 7 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 3〈/p〉 〈p〉Author(s): Anne L. Collins, Amy R. Wolff, Benjamin T. Saunders〈/p〉 〈div〉〈p〉A recent 〈em〉Cell〈/em〉 paper identifies a novel population of neurons within the ventral tegmental area producing the endogenous opioid nociceptin that regulates dopamine neuron firing and acts uniquely to gate motivation in reward seeking. These results highlight neuropeptidergic signaling as a critical component of functional heterogeneity in the midbrain.〈/p〉〈/div〉
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    Cerebral Microvascular Injury: A Potentially Treatable Endophenotype of Traumatic Brain Injury-Induced Neurodegeneration (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 7 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 3〈/p〉 〈p〉Author(s): Danielle K. Sandsmark, Asma Bashir, Cheryl L. Wellington, Ramon Diaz-Arrastia〈/p〉 〈div〉〈p〉Traumatic brain injury (TBI) is one the most common human afflictions, contributing to long-term disability in survivors. Emerging data indicate that functional improvement or deterioration can occur years after TBI. In this regard, TBI is recognized as risk factor for late-life neurodegenerative disorders. TBI encompasses a heterogeneous disease process in which diverse injury subtypes and multiple molecular mechanisms overlap. To develop precision medicine approaches where specific pathobiological processes are targeted by mechanistically appropriate therapies, techniques to identify and measure these subtypes are needed. Traumatic microvascular injury is a common but relatively understudied TBI endophenotype. In this review, we describe evidence of microvascular dysfunction in human and animal TBI, explore the role of vascular dysfunction in neurodegenerative disease, and discuss potential opportunities for vascular-directed therapies in ameliorating TBI-related neurodegeneration. We discuss the therapeutic potential of vascular-directed therapies in TBI and the use and limitations of preclinical models to explore these therapies.〈/p〉〈/div〉
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    A Role of Drd2 Hippocampal Neurons in Context-Dependent Food Intake (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 28 March 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Estefania P. Azevedo, Lisa Pomeranz, Jia Cheng, Marc Schneeberger, Roger Vaughan, Sarah A. Stern, Bowen Tan, Katherine Doerig, Paul Greengard, Jeffrey M. Friedman〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Associative learning of food cues that link location in space to food availability guides feeding behavior in mammals. However, the function of specific neurons that are elements of the higher-order, cognitive circuitry controlling feeding behavior is largely unexplored. Here, we report that hippocampal dopamine 2 receptor (hD2R) neurons are specifically activated by food and that both acute and chronic modulation of their activity reduces food intake in mice. Upstream projections from the lateral entorhinal cortex (LEC) to the hippocampus activate hD2R cells and can also decrease food intake. Finally, activation of hD2R neurons interferes with the encoding of a spatial memory linking food to a specific location via projections from the hippocampus to the septal area. Altogether these data describe a previously unidentified LEC 〉 hippocampus 〉 septal higher-order circuit that regulates feeding behavior.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627319302181-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    Location and Plasticity of the Sodium Spike Initiation Zone in Nociceptive Terminals In Vivo (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 26 March 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Robert H. Goldstein, Omer Barkai, Almudena Íñigo-Portugués, Ben Katz, Shaya Lev, Alexander M. Binshtok〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Nociceptive terminals possess the elements for detecting, transmitting, and modulating noxious signals, thus being pivotal for pain sensation. Despite this, a functional description of the transduction process by the terminals, in physiological conditions, has not been fully achieved. Here, we studied how nociceptive terminals 〈em〉in vivo〈/em〉 convert noxious stimuli into propagating signals. By monitoring noxious-stimulus-induced Ca〈sup〉2+〈/sup〉 dynamics from mouse corneal terminals, we found that initiation of Na〈sup〉+〈/sup〉 channel (Nav)-dependent propagating signals takes place away from the terminal and that the starting point for Nav-mediated propagation depends on Nav functional availability. Acute treatment with the proinflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) resulted in a shift of the location of Nav involvement toward the terminal, thus increasing nociceptive excitability. Moreover, a shift of Nav involvement toward the terminal occurs in corneal hyperalgesia resulting from acute photokeratitis. This dynamic change in the location of Nav-mediated propagation initiation could underlie pathological pain hypersensitivity.〈/p〉〈/div〉
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    A Genetically Encoded Fluorescent Sensor for Rapid and Specific In Vivo Detection of Norepinephrine (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 25 March 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Jiesi Feng, Changmei Zhang, Julieta E. Lischinsky, Miao Jing, Jingheng Zhou, Huan Wang, Yajun Zhang, Ao Dong, Zhaofa Wu, Hao Wu, Weiyu Chen, Peng Zhang, Jing Zou, S. Andrew Hires, J. Julius Zhu, Guohong Cui, Dayu Lin, Jiulin Du, Yulong Li〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Norepinephrine (NE) is a key biogenic monoamine neurotransmitter involved in a wide range of physiological processes. However, its precise dynamics and regulation remain poorly characterized, in part due to limitations of available techniques for measuring NE 〈em〉in vivo〈/em〉. Here, we developed a family of GPCR activation-based NE (GRAB〈sub〉NE〈/sub〉) sensors with a 230% peak ΔF/F〈sub〉0〈/sub〉 response to NE, good photostability, nanomolar-to-micromolar sensitivities, sub-second kinetics, and high specificity. Viral- or transgenic-mediated expression of GRAB〈sub〉NE〈/sub〉 sensors was able to detect electrical-stimulation-evoked NE release in the locus coeruleus (LC) of mouse brain slices, looming-evoked NE release in the midbrain of live zebrafish, as well as optogenetically and behaviorally triggered NE release in the LC and hypothalamus of freely moving mice. Thus, GRAB〈sub〉NE〈/sub〉 sensors are robust tools for rapid and specific monitoring of 〈em〉in vivo〈/em〉 NE transmission in both physiological and pathological processes.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627319301722-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    α1ACT Is Essential for Survival and Early Cerebellar Programming in a Critical Neonatal Window (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 25 March 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Xiaofei Du, Cenfu Wei, Daniel Parviz Hejazi Pastor, Eshaan R. Rao, Yan Li, Giorgio Grasselli, Jack Godfrey, Ann C. Palmenberg, Jorge Andrade, Christian Hansel, Christopher M. Gomez〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Postnatal cerebellar development is a precisely regulated process involving well-orchestrated expression of neural genes. Neurological phenotypes associated with 〈em〉CACNA1A〈/em〉 gene defects have been increasingly recognized, yet the molecular principles underlying this association remain elusive. By characterizing a dose-dependent 〈em〉CACNA1A〈/em〉 gene deficiency mouse model, we discovered that α1ACT, as a transcription factor and secondary protein of 〈em〉CACNA1A〈/em〉 mRNA, drives dynamic gene expression networks within cerebellar Purkinje cells and is indispensable for neonatal survival. Perinatal loss of α1ACT leads to motor dysfunction through disruption of neurogenesis and synaptic regulatory networks. However, its elimination in adulthood has minimal effect on the cerebellum. These findings shed light on the critical role of α1ACT in facilitating neuronal development in both mice and humans and support a rationale for gene therapies for calcium-channel-associated cerebellar disorders. Finally, we show that bicistronic expression may be common to the voltage-gated calcium channel (VGCC) gene family and may help explain complex genetic syndromes.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627319301710-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    Conversion of Graded Presynaptic Climbing Fiber Activity into Graded Postsynaptic Ca2+ Signals by Purkinje Cell Dendrites (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 27 March 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Michael A. Gaffield, Audrey Bonnan, Jason M. Christie〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉The brain must make sense of external stimuli to generate relevant behavior. We used a combination of 〈em〉in vivo〈/em〉 approaches to investigate how the cerebellum processes sensory-related information. We found that the inferior olive encodes contexts of sensory-associated external cues in a graded manner, apparent in the presynaptic activity of their axonal projections (climbing fibers) in the cerebellar cortex. Individual climbing fibers were broadly responsive to different sensory modalities but relayed sensory-related information to the cortex in a lobule-dependent manner. Purkinje cell dendrites faithfully transformed this climbing fiber activity into dendrite-wide Ca〈sup〉2+〈/sup〉 signals without a direct contribution from the mossy fiber pathway. These results demonstrate that the size of climbing-fiber-evoked Ca〈sup〉2+〈/sup〉 signals in Purkinje cell dendrites is largely determined by the firing level of climbing fibers. This coding scheme emphasizes the overwhelming role of the inferior olive in generating salient signals useful for instructing plasticity and learning.〈/p〉〈/div〉
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    Mechanisms Underlying Microbial-Mediated Changes in Social Behavior in Mouse Models of Autism Spectrum Disorder (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 16 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 2〈/p〉 〈p〉Author(s): Martina Sgritta, Sean W. Dooling, Shelly A. Buffington, Eric N. Momin, Michael B. Francis, Robert A. Britton, Mauro Costa-Mattioli〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Currently, there are no medications that effectively treat the core symptoms of Autism Spectrum Disorder (ASD). We recently found that the bacterial species 〈em〉Lactobacillus (L.) reuteri〈/em〉 reverses social deficits in maternal high-fat-diet offspring. However, whether the effect of 〈em〉L. reuteri〈/em〉 on social behavior is generalizable to other ASD models and its mechanism(s) of action remains unknown. Here, we found that treatment with 〈em〉L. reuteri〈/em〉 selectively rescues social deficits in genetic, environmental, and idiopathic ASD models. Interestingly, the effects of 〈em〉L. reuteri〈/em〉 on social behavior are not mediated by restoring the composition of the host’s gut microbiome, which is altered in all of these ASD models. Instead, 〈em〉L. reuteri〈/em〉 acts in a vagus nerve-dependent manner and rescues social interaction-induced synaptic plasticity in the ventral tegmental area of ASD mice, but not in oxytocin receptor-deficient mice. Collectively, treatment with 〈em〉L. reuteri〈/em〉 emerges as promising non-invasive microbial-based avenue to combat ASD-related social dysfunction.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627318310092-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    The NeuroDev Study: Phenotypic and Genetic Characterization of Neurodevelopmental Disorders in Kenya and South Africa (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 2 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 1〈/p〉 〈p〉Author(s): Victoria de Menil, Michelle Hoogenhout, Patricia Kipkemoi, Dorcas Kamuya, Emma Eastman, Alice Galvin, Katini Mwangasha, Jantina de Vries, Symon M. Kariuki, Serini Murugasen, Paul Mwangi, Ilina Singh, Dan J. Stein, Amina Abubakar, Charles R. Newton, Kirsten A. Donald, Elise Robinson〈/p〉 〈div〉〈p〉The NeuroDev study will deeply phenotype cognition, behavior, dysmorphias, and neuromedical traits on an expected cohort of 5,600 Africans (1,800 child cases, 1,800 child controls, and 1,900 parents) and will collect whole blood for exome sequencing and biobanking.〈/p〉〈/div〉
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    Mechanisms of Spatiotemporal Selectivity in Cortical Area MT (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 6 February 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 3〈/p〉 〈p〉Author(s): Ambarish S. Pawar, Sergei Gepshtein, Sergey Savel’ev, Thomas D. Albright〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Cortical sensory neurons are characterized by selectivity to stimulation. This selectivity was originally viewed as a part of the fundamental “receptive field” characteristic of neurons. This view was later challenged by evidence that receptive fields are modulated by stimuli outside of the classical receptive field. Here, we show that even this modified view of selectivity needs revision. We measured spatial frequency selectivity of neurons in cortical area MT of alert monkeys and found that their selectivity strongly depends on luminance contrast, shifting to higher spatial frequencies as contrast increases. The changes of preferred spatial frequency are large at low temporal frequency, and they decrease monotonically as temporal frequency increases. That is, even interactions among basic stimulus dimensions of luminance contrast, spatial frequency, and temporal frequency strongly influence neuronal selectivity. This dynamic nature of neuronal selectivity is inconsistent with the notion of stimulus preference as a stable characteristic of cortical neurons.〈/p〉〈/div〉
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    Developmental Heterogeneity of Microglia and Brain Myeloid Cells Revealed by Deep Single-Cell RNA Sequencing (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 16 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 2〈/p〉 〈p〉Author(s): Qingyun Li, Zuolin Cheng, Lu Zhou, Spyros Darmanis, Norma F. Neff, Jennifer Okamoto, Gunsagar Gulati, Mariko L. Bennett, Lu O. Sun, Laura E. Clarke, Julia Marschallinger, Guoqiang Yu, Stephen R. Quake, Tony Wyss-Coray, Ben A. Barres〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Microglia are increasingly recognized for their major contributions during brain development and neurodegenerative disease. It is currently unknown whether these functions are carried out by subsets of microglia during different stages of development and adulthood or within specific brain regions. Here, we performed deep single-cell RNA sequencing (scRNA-seq) of microglia and related myeloid cells sorted from various regions of embryonic, early postnatal, and adult mouse brains. We found that the majority of adult microglia expressing homeostatic genes are remarkably similar in transcriptomes, regardless of brain region. By contrast, early postnatal microglia are more heterogeneous. We discovered a proliferative-region-associated microglia (PAM) subset, mainly found in developing white matter, that shares a characteristic gene signature with degenerative disease-associated microglia (DAM). Such PAM have amoeboid morphology, are metabolically active, and phagocytose newly formed oligodendrocytes. This scRNA-seq atlas will be a valuable resource for dissecting innate immune functions in health and disease.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627318310821-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    Mutations in Chromatin Modifier and Ephrin Signaling Genes in Vein of Galen Malformation (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 6 February 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 3〈/p〉 〈p〉Author(s): Daniel Duran, Xue Zeng, Sheng Chih Jin, Jungmin Choi, Carol Nelson-Williams, Bogdan Yatsula, Jonathan Gaillard, Charuta Gavankar Furey, Qiongshi Lu, Andrew T. Timberlake, Weilai Dong, Michelle A. Sorscher, Erin Loring, Jennifer Klein, August Allocco, Ava Hunt, Sierra Conine, Jason K. Karimy, Mark W. Youngblood, Jinwei Zhang〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Normal vascular development includes the formation and specification of arteries, veins, and intervening capillaries. Vein of Galen malformations (VOGMs) are among the most common and severe neonatal brain arterio-venous malformations, shunting arterial blood into the brain’s deep venous system through aberrant direct connections. Exome sequencing of 55 VOGM probands, including 52 parent-offspring trios, revealed enrichment of rare damaging 〈em〉de novo〈/em〉 mutations in chromatin modifier genes that play essential roles in brain and vascular development. Other VOGM probands harbored rare inherited damaging mutations in Ephrin signaling genes, including a genome-wide significant mutation burden in 〈em〉EPHB4〈/em〉. Inherited mutations showed incomplete penetrance and variable expressivity, with mutation carriers often exhibiting cutaneous vascular abnormalities, suggesting a two-hit mechanism. The identified mutations collectively account for ∼30% of studied VOGM cases. These findings provide insight into disease biology and may have clinical implications for risk assessment.〈/p〉〈/div〉
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    Tac1-Expressing Neurons in the Periaqueductal Gray Facilitate the Itch-Scratching Cycle via Descending Regulation (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 2 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 1〈/p〉 〈p〉Author(s): Zheng-Run Gao, Wen-Zhen Chen, Ming-Zhe Liu, Xiao-Jun Chen, Li Wan, Xin-Yan Zhang, Lei Yuan, Jun-Kai Lin, Meng Wang, Li Zhou, Xiao-Hong Xu, Yan-Gang Sun〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Uncontrollable itch-scratching cycles lead to serious skin damage in patients with chronic itch. However, the neural mechanism promoting the itch-scratching cycle remains elusive. Here, we report that tachykinin 1 (Tac1)-expressing glutamatergic neurons in the lateral and ventrolateral periaqueductal gray (l/vlPAG) facilitate the itch-scratching cycle. We found that l/vlPAG neurons exhibited scratching-behavior-related neural activity and that itch-evoked scratching behavior was impaired after suppressing the activity of l/vlPAG neurons. Furthermore, we showed that the activity of Tac1-expressing glutamatergic neurons in the l/vlPAG was elevated during itch-induced scratching behavior and that ablating or suppressing the activity of these neurons decreased itch-induced scratching behavior. Importantly, activation of Tac1-expressing neurons induced robust spontaneous scratching and grooming behaviors. The scratching behavior evoked by Tac1-expressing neuron activation was suppressed by ablation of spinal neurons expressing gastrin-releasing peptide receptor (GRPR), the key relay neurons for itch. These results suggest that Tac1-expressing neurons in the l/vlPAG promote itch-scratching cycles.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627318310018-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    The Costs of Reproducibility (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 2 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 1〈/p〉 〈p〉Author(s): Russell A. Poldrack〈/p〉 〈div〉〈p〉Improving the reproducibility of neuroscience research is of great concern, especially to early-career researchers (ECRs). Here I outline the potential costs for ECRs in adopting practices to improve reproducibility. I highlight the ways in which ECRs can achieve their career goals while doing better science and the need for established researchers to support them in these efforts.〈/p〉〈/div〉
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    Suppressing Memories by Shrinking the Vesicle Pool (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 2 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 1〈/p〉 〈p〉Author(s): Ethan B. Richman, Liqun Luo〈/p〉 〈div〉〈p〉The cohesin complex regulates cellular functions spanning cell division and neuronal morphogenesis. Now, Phan et al. uncover a role for the cohesin complex in regulating memory acquisition and the size of the synaptic and dense-core vesicle pool.〈/p〉〈/div〉
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    Scenes in the Human Brain: Comparing 2D versus 3D Representations (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 2 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 1〈/p〉 〈p〉Author(s): Iris I.A. Groen, Chris I. Baker〈/p〉 〈div〉〈p〉Three cortical brain regions are thought to underlie our remarkable ability to perceive and understand visual scenes. In this issue of 〈em〉Neuron〈/em〉, Lescroart and Gallant (2018) use quantitative models of scene processing to reveal 3D representations in these regions.〈/p〉〈/div〉
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    Sodium Is Detected by the OVLT to Regulate Sympathetic Tone (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 2 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 1〈/p〉 〈p〉Author(s): Patrice G. Guyenet〈/p〉 〈div〉〈p〉Hypernatremia is known to elicit a rise in sympathetic tone and blood pressure. In this issue of 〈em〉Neuron〈/em〉, Nomura et al. (2018) now show that this is mediated via the organum vasculosum laminae terminalis (OVLT). Na〈sup〉+〈/sup〉 activates OVLT neurons via a paracrine mechanism involving sodium channel Na〈sub〉x〈/sub〉 expressed by astrocytes and the ependyma.〈/p〉〈/div〉
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    Interactive Regulation of Neuronal Development by Hippocampal Stem Cell Niche Populations (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 2 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 1〈/p〉 〈p〉Author(s): J.E. Le Belle, H.I. Kornblum〈/p〉 〈div〉〈p〉Microenvironment cues and cell-to-cell interactions balance stem cell quiescence with proliferation and direct neurogenesis in the adult hippocampal niche. Tang et al. report that hippocampal stem cells release feedback signals that regulate the dendritic complexity and activity of newborn neurons.〈/p〉〈/div〉
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    A Dendritic Substrate for the Cholinergic Control of Neocortical Output Neurons (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 6 February 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 3〈/p〉 〈p〉Author(s): Stephen R. Williams, Lee N. Fletcher〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉The ascending cholinergic system dynamically regulates sensory perception and cognitive function, but it remains unclear how this modulation is executed in neocortical circuits. Here, we demonstrate that the cholinergic system controls the integrative operations of neocortical principal neurons by modulating dendritic excitability. Direct dendritic recordings revealed that the optogenetic-evoked release of acetylcholine (ACh) transformed the pattern of dendritic integration in layer 5B pyramidal neurons, leading to the generation of dendritic plateau potentials which powerfully drove repetitive action potential output. In contrast, the synaptic release of ACh did not positively modulate axo-somatic excitability. Mechanistically, the transformation of dendritic integration was mediated by the muscarinic ACh receptor-dependent enhancement of dendritic R-type calcium channel activity, a compartment-dependent modulation which decisively controlled the associative computations executed by layer 5B pyramidal neurons. Our findings therefore reveal a biophysical mechanism by which the cholinergic system controls dendritic computations causally linked to perceptual detection.〈/p〉〈/div〉
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    The Hippocampus and Neocortical Inhibitory Engrams Protect against Memory Interference (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 6 February 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 3〈/p〉 〈p〉Author(s): Renée S. Koolschijn, Uzay E. Emir, Alexandros C. Pantelides, Hamed Nili, Timothy E.J. Behrens, Helen C. Barron〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Our experiences often overlap with each other, yet we are able to selectively recall individual memories to guide decisions and future actions. The neural mechanisms that support such precise memory recall remain unclear. Here, using ultra-high field 7T MRI we reveal two distinct mechanisms that protect memories from interference. The first mechanism involves the hippocampus, where the blood-oxygen-level-dependent (BOLD) signal predicts behavioral measures of memory interference, and representations of context-dependent memories are pattern separated according to their relational overlap. The second mechanism involves neocortical inhibition. When we reduce the concentration of neocortical GABA using trans-cranial direct current stimulation (tDCS), neocortical memory interference increases in proportion to the reduction in GABA, which in turn predicts behavioral performance. These findings suggest that memory interference is mediated by both the hippocampus and neocortex, where the hippocampus separates overlapping but context-dependent memories using relational information, and neocortical inhibition prevents unwanted co-activation between overlapping memories.〈/p〉〈/div〉
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    Circuit Models of Low-Dimensional Shared Variability in Cortical Networks (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 16 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 2〈/p〉 〈p〉Author(s): Chengcheng Huang, Douglas A. Ruff, Ryan Pyle, Robert Rosenbaum, Marlene R. Cohen, Brent Doiron〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Trial-to-trial variability is a reflection of the circuitry and cellular physiology that make up a neuronal network. A pervasive yet puzzling feature of cortical circuits is that despite their complex wiring, population-wide shared spiking variability is low dimensional. Previous model cortical networks cannot explain this global variability, and rather assume it is from external sources. We show that if the spatial and temporal scales of inhibitory coupling match known physiology, networks of model spiking neurons internally generate low-dimensional shared variability that captures population activity recorded 〈em〉in vivo〈/em〉. Shifting spatial attention into the receptive field of visual neurons has been shown to differentially modulate shared variability within and between brain areas. A top-down modulation of inhibitory neurons in our network provides a parsimonious mechanism for this attentional modulation. Our work provides a critical link between observed cortical circuit structure and realistic shared neuronal variability and its modulation.〈/p〉〈/div〉
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    Migraine-Associated TRESK Mutations Increase Neuronal Excitability through Alternative Translation Initiation and Inhibition of TREK (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 16 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 2〈/p〉 〈p〉Author(s): Perrine Royal, Alba Andres-Bilbe, Pablo Ávalos Prado, Clément Verkest, Brigitte Wdziekonski, Sébastien Schaub, Anne Baron, Florian Lesage, Xavier Gasull, Joshua Levitz, Guillaume Sandoz〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉It is often unclear why some genetic mutations to a given gene contribute to neurological disorders and others do not. For instance, two mutations have previously been found to produce a dominant negative for TRESK, a two-pore-domain K+ channel implicated in migraine: TRESK-MT, a 2-bp frameshift mutation, and TRESK-C110R. Both mutants inhibit TRESK, but only TRESK-MT increases sensory neuron excitability and is linked to migraine. Here, we identify a new mechanism, termed frameshift mutation-induced alternative translation initiation (fsATI), that may explain why only TRESK-MT is associated with migraine. fsATI leads to the production of a second protein fragment, TRESK-MT2, which co-assembles with and inhibits TREK1 and TREK2, two other two-pore-domain K+ channels, to increase trigeminal sensory neuron excitability, leading to a migraine-like phenotype in rodents. These findings identify TREK1 and TREK2 as potential molecular targets in migraine and suggest that fsATI should be considered as a distinct class of mutations.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627318310481-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    Axoglial Adhesion by Cadm4 Regulates CNS Myelination (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 16 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 2〈/p〉 〈p〉Author(s): Nimrod Elazar, Anya Vainshtein, Neev Golan, Bharath Vijayaragavan, Nicole Schaeren-Wiemers, Yael Eshed-Eisenbach, Elior Peles〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉The initiation of axoglial contact is considered a prerequisite for myelination, yet the role cell adhesion molecules (CAMs) play in mediating such interactions remains unclear. To examine the function of axoglial CAMs, we tested whether enhanced CAM-mediated adhesion between OLs and neurons could affect myelination. Here we show that increased expression of a membrane-bound extracellular domain of Cadm4 (Cadm4dCT) in cultured oligodendrocytes results in the production of numerous axoglial contact sites that fail to elongate and generate mature myelin. Transgenic mice expressing Cadm4dCT were hypomyelinated and exhibit multiple myelin abnormalities, including myelination of neuronal somata. These abnormalities depend on specific neuron-glial interaction as they were not observed when these OLs were cultured alone, on nanofibers, or on neurons isolated from mice lacking the axonal receptors of Cadm4. Our results demonstrate that tightly regulated axon-glia adhesion is essential for proper myelin targeting and subsequent membrane wrapping and lateral extension.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627318310419-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    Engram Cell Excitability State Determines the Efficacy of Memory Retrieval (2019)
    Elsevier
    In: Neuron
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    Publication Date: 2019
    Description: 〈p〉Publication date: 16 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 2〈/p〉 〈p〉Author(s): Michele Pignatelli, Tomás J. Ryan, Dheeraj S. Roy, Chanel Lovett, Lillian M. Smith, Shruti Muralidhar, Susumu Tonegawa〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Animals need to optimize the efficacy of memory retrieval to adapt to environmental circumstances for survival. The recent development of memory engram labeling technology allows a precise investigation of the processes associated with the recall of a specific memory. Here, we show that engram cell excitability is transiently increased following memory reactivation. This short-term increase of engram excitability enhances the subsequent retrieval of specific memory content in response to cues and is manifest in the animal’s ability to recognize contexts more precisely and more effectively. These results reveal a hitherto unknown transient enhancement of context recognition based on the plasticity of engram cell excitability. They also suggest that recall of a contextual memory is influenced by previous but recent activation of the same engram. The state of excitability of engram cells mediates differential behavioral outcomes upon memory retrieval and may be crucial for survival by promoting adaptive behavior.〈/p〉〈/div〉
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    CaV2.1 α1 Subunit Expression Regulates Presynaptic CaV2.1 Abundance and Synaptic Strength at a Central Synapse (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 16 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 2〈/p〉 〈p〉Author(s): Matthias Lübbert, R. Oliver Goral, Christian Keine, Connon Thomas, Debbie Guerrero-Given, Travis Putzke, Rachel Satterfield, Naomi Kamasawa, Samuel M. Young〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉The abundance of presynaptic Ca〈sub〉V〈/sub〉2 voltage-gated Ca〈sup〉2+〈/sup〉 channels (Ca〈sub〉V〈/sub〉2) at mammalian active zones (AZs) regulates the efficacy of synaptic transmission. It is proposed that presynaptic Ca〈sub〉V〈/sub〉2 levels are saturated in AZs due to a finite number of slots that set Ca〈sub〉V〈/sub〉2 subtype abundance and that Ca〈sub〉V〈/sub〉2.1 cannot compete for Ca〈sub〉V〈/sub〉2.2 slots. However, at most AZs, Ca〈sub〉V〈/sub〉2.1 levels are highest and Ca〈sub〉V〈/sub〉2.2 levels are developmentally reduced. To investigate Ca〈sub〉V〈/sub〉2.1 saturation states and preference in AZs, we overexpressed the Ca〈sub〉V〈/sub〉2.1 and Ca〈sub〉V〈/sub〉2.2 α〈sub〉1〈/sub〉 subunits at the calyx of Held at immature and mature developmental stages. We found that AZs prefer Ca〈sub〉V〈/sub〉2.1 to Ca〈sub〉V〈/sub〉2.2. Remarkably, Ca〈sub〉V〈/sub〉2.1 α〈sub〉1〈/sub〉 subunit overexpression drove increased Ca〈sub〉V〈/sub〉2.1 currents and channel numbers and increased synaptic strength at both developmental stages examined. Therefore, we propose that Ca〈sub〉V〈/sub〉2.1 levels in the AZ are not saturated and that synaptic strength can be modulated by increasing Ca〈sub〉V〈/sub〉2.1 levels to regulate neuronal circuit output.〈/p〉〈/div〉 〈div〉 〈h6〉Video Abstract〈/h6〉 〈p〉〈/p〉 〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627318310377-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    Activity of Prefrontal Neurons Predict Future Choices during Gambling (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 2 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 1〈/p〉 〈p〉Author(s): Johannes Passecker, Nace Mikus, Hugo Malagon-Vina, Philip Anner, Jordane Dimidschstein, Gordon Fishell, Georg Dorffner, Thomas Klausberger〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Neuronal signals in the prefrontal cortex have been reported to predict upcoming decisions. Such activity patterns are often coupled to perceptual cues indicating correct choices or values of different options. How does the prefrontal cortex signal future decisions when no cues are present but when decisions are made based on internal valuations of past experiences with stochastic outcomes? We trained rats to perform a two-arm bandit-task, successfully adjusting choices between certain-small or possible-big rewards with changing long-term advantages. We discovered specialized prefrontal neurons, whose firing during the encounter of no-reward predicted the subsequent choice of animals, even for unlikely or uncertain decisions and several seconds before choice execution. Optogenetic silencing of the prelimbic cortex exclusively timed to encounters of no reward, provoked animals to excessive gambling for large rewards. Firing of prefrontal neurons during outcome evaluation signals subsequent choices during gambling and is essential for dynamically adjusting decisions based on internal valuations.〈/p〉〈/div〉
    Print ISSN: 0896-6273
    Electronic ISSN: 1097-4199
    Topics: Biology , Medicine
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    Fractionating Blunted Reward Processing Characteristic of Anhedonia by Over-Activating Primate Subgenual Anterior Cingulate Cortex (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 16 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 2〈/p〉 〈p〉Author(s): Laith Alexander, Philip L.R. Gaskin, Stephen J. Sawiak, Tim D. Fryer, Young T. Hong, Gemma J. Cockcroft, Hannah F. Clarke, Angela C. Roberts〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Anhedonia is a core symptom of depression, but the underlying neurobiological mechanisms are unknown. Correlative neuroimaging studies implicate dysfunction within ventromedial prefrontal cortex, but the causal roles of specific subregions remain unidentified. We addressed these issues by combining intracerebral microinfusions with cardiovascular and behavioral monitoring in marmoset monkeys to show that over-activation of primate subgenual anterior cingulate cortex (sgACC, area 25) blunts appetitive anticipatory, but not consummatory, arousal, whereas manipulations of adjacent perigenual ACC (pgACC, area 32) have no effect. sgACC/25 over-activation also reduces the willingness to work for reward. 〈sup〉18〈/sup〉F-FDG PET imaging reveals over-activation induced metabolic changes in circuits involved in reward processing and interoception. Ketamine treatment ameliorates the blunted anticipatory arousal and reverses associated metabolic changes. These results demonstrate a causal role for primate sgACC/25 over-activity in selective aspects of impaired reward processing translationally relevant to anhedonia, and ketamine’s modulation of an affective network to exert its action.〈/p〉〈/div〉
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    How the Internally Organized Direction Sense Is Used to Navigate (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 16 January 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 101, Issue 2〈/p〉 〈p〉Author(s): Eun Hye Park, Stephen Keeley, Cristina Savin, James B. Ranck, André A. Fenton〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Head-direction cells preferentially discharge when the head points in a particular azimuthal direction, are hypothesized to collectively function as a single neural system for a unitary direction sense, and are believed to be essential for navigating extra-personal space by functioning like a compass. We tested these ideas by recording medial entorhinal cortex (MEC) head-direction cells while rats navigated on a familiar, continuously rotating disk that dissociates the environment into two spatial frames: one stationary and one rotating. Head-direction cells degraded directional tuning referenced to either of the externally referenced spatial frames, but firing rates, sub-second cell-pair action potential discharge relationships, and internally referenced directional tuning were preserved. MEC head-direction cell ensemble discharge collectively generates a subjective, internally referenced unitary representation of direction that, unlike a compass, is inconsistently registered to external landmarks during navigation. These findings indicate that MEC-based directional information is subjectively anchored, potentially providing for navigation without a stable externally anchored direction sense.〈/p〉〈/div〉 〈div〉 〈h6〉Video Abstract〈/h6〉 〈p〉〈/p〉 〈/div〉
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    Inhibition of Axon Regeneration by Liquid-like TIAR-2 Granules (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 1 August 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Matthew G. Andrusiak, Panid Sharifnia, Xiaohui Lyu, Zhiping Wang, Andrea M. Dickey, Zilu Wu, Andrew D. Chisholm, Yishi Jin〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Phase separation into liquid-like compartments is an emerging property of proteins containing prion-like domains (PrLDs), yet the 〈em〉in vivo〈/em〉 roles of phase separation remain poorly understood. TIA proteins contain a C-terminal PrLD, and mutations in the PrLD are associated with several diseases. Here, we show that the 〈em〉C. elegans〈/em〉 TIAR-2/TIA protein functions cell autonomously to inhibit axon regeneration. TIAR-2 undergoes liquid-liquid phase separation 〈em〉in vitro〈/em〉 and forms granules with liquid-like properties 〈em〉in vivo〈/em〉. Axon injury induces a transient increase in TIAR-2 granule number. The PrLD is necessary and sufficient for granule formation and inhibiting regeneration. Tyrosine residues within the PrLD are important for granule formation and inhibition of regeneration. TIAR-2 is also serine phosphorylated 〈em〉in vivo〈/em〉. Non-phosphorylatable TIAR-2 variants do not form granules and are unable to inhibit axon regeneration. Our data demonstrate an 〈em〉in vivo〈/em〉 function for phase-separated TIAR-2 and identify features critical for its function in axon regeneration.〈/p〉〈/div〉 〈h5〉Graphical Abstract〈/h5〉 〈div〉〈p〉〈figure〉〈img src="https://ars.els-cdn.com/content/image/1-s2.0-S0896627319306026-fx1.jpg" width="375" alt="Graphical abstract for this article" title=""〉〈/figure〉〈/p〉〈/div〉
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    Task-Dependent Changes in the Large-Scale Dynamics and Necessity of Cortical Regions (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: Available online 26 September 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron〈/p〉 〈p〉Author(s): Lucas Pinto, Kanaka Rajan, Brian DePasquale, Stephan Y. Thiberge, David W. Tank, Carlos D. Brody〈/p〉 〈h5〉Summary〈/h5〉 〈div〉〈p〉Neural activity throughout the cortex is correlated with perceptual decisions, but inactivation studies suggest that only a small number of areas are necessary for these behaviors. Here we show that the number of required cortical areas and their dynamics vary across related tasks with different cognitive computations. In a visually guided virtual T-maze task, bilateral inactivation of only a few dorsal cortical regions impaired performance. In contrast, in tasks requiring evidence accumulation and/or post-stimulus memory, performance was impaired by inactivation of widespread cortical areas with diverse patterns of behavioral deficits across areas and tasks. Wide-field imaging revealed widespread ramps of Ca〈sup〉2+〈/sup〉 activity during the accumulation and visually guided tasks. Additionally, during accumulation, different regions had more diverse activity profiles, leading to reduced inter-area correlations. Using a modular recurrent neural network model trained to perform analogous tasks, we argue that differences in computational strategies alone could explain these findings.〈/p〉〈/div〉
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    Becoming a Principal Investigator: Designing and Navigating Your Academic Adventure (2019)
    Elsevier
    In: Neuron
    Details
    Publication Date: 2019
    Description: 〈p〉Publication date: 25 September 2019〈/p〉 〈p〉〈b〉Source:〈/b〉 Neuron, Volume 103, Issue 6〈/p〉 〈p〉Author(s): Paul L. Greer, Melanie A. Samuel〈/p〉 〈div〉〈p〉Starting your own academic lab is a wonderful opportunity to impact science through research and trainee mentoring. In this article, we share some thoughts and resources for this undertaking in the hope that they may enhance the experience of others.〈/p〉〈/div〉
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