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  • 1
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    Reversal of cocaine-evoked synaptic potentiation resets drug-induced adaptive behaviour (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-12-14
    Description: Drug-evoked synaptic plasticity is observed at many synapses and may underlie behavioural adaptations in addiction. Mechanistic investigations start with the identification of the molecular drug targets. Cocaine, for example, exerts its reinforcing and early neuroadaptive effects by inhibiting the dopamine transporter, thus causing a strong increase in mesolimbic dopamine. Among the many signalling pathways subsequently engaged, phosphorylation of the extracellular signal-regulated kinase (ERK) in the nucleus accumbens is of particular interest because it has been implicated in NMDA-receptor and type 1 dopamine (D1)-receptor-dependent synaptic potentiation as well as in several behavioural adaptations. A causal link between drug-evoked plasticity at identified synapses and behavioural adaptations, however, is missing, and the benefits of restoring baseline transmission have yet to be demonstrated. Here we find that cocaine potentiates excitatory transmission in D1-receptor-expressing medium-sized spiny neurons (D1R-MSNs) in mice via ERK signalling with a time course that parallels locomotor sensitization. Depotentiation of cortical nucleus accumbens inputs by optogenetic stimulation in vivo efficiently restored normal transmission and abolished cocaine-induced locomotor sensitization. These findings establish synaptic potentiation selectively in D1R-MSNs as a mechanism underlying a core component of addiction, probably by creating an imbalance between distinct populations of MSNs in the nucleus accumbens. Our data also provide proof of principle that reversal of cocaine-evoked synaptic plasticity can treat behavioural alterations caused by addictive drugs and may inspire novel therapeutic approaches involving deep brain stimulation or transcranial magnetic stimulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pascoli, Vincent -- Turiault, Marc -- Luscher, Christian -- England -- Nature. 2011 Dec 7;481(7379):71-5. doi: 10.1038/nature10709.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Basic Neurosciences, Medical Faculty, University of Geneva, CH-1211 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22158102" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/drug effects ; Animals ; Cocaine/administration & dosage/*pharmacology ; Cocaine-Related Disorders/metabolism/pathology ; Dopaminergic Neurons/drug effects/metabolism ; Electric Stimulation ; Enzyme Activation ; Excitatory Postsynaptic Potentials/drug effects ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Injections ; Long-Term Potentiation/drug effects ; MAP Kinase Signaling System/drug effects ; Mice ; Mice, Inbred C57BL ; Motor Activity/drug effects ; Neuronal Plasticity/drug effects ; Nucleus Accumbens/cytology/drug effects ; Phenotype ; Receptors, Dopamine D1/metabolism ; Synapses/drug effects/metabolism ; Synaptic Transmission/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Contrasting forms of cocaine-evoked plasticity control components of relapse (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-05-23
    Description: Nucleus accumbens neurons serve to integrate information from cortical and limbic regions to direct behaviour. Addictive drugs are proposed to hijack this system, enabling drug-associated cues to trigger relapse to drug seeking. However, the connections affected and proof of causality remain to be established. Here we use a mouse model of delayed cue-associated cocaine seeking with ex vivo electrophysiology in optogenetically delineated circuits. We find that seeking correlates with rectifying AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptor transmission and a reduced AMPA/NMDA (N-methyl-D-aspartate) ratio at medial prefrontal cortex (mPFC) to nucleus accumbens shell D1-receptor medium-sized spiny neurons (D1R-MSNs). In contrast, the AMPA/NMDA ratio increases at ventral hippocampus to D1R-MSNs. Optogenetic reversal of cocaine-evoked plasticity at both inputs abolishes seeking, whereas selective reversal at mPFC or ventral hippocampus synapses impairs response discrimination or reduces response vigour during seeking, respectively. Taken together, we describe how information integration in the nucleus accumbens is commandeered by cocaine at discrete synapses to allow relapse. Our approach holds promise for identifying synaptic causalities in other behavioural disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pascoli, Vincent -- Terrier, Jean -- Espallergues, Julie -- Valjent, Emmanuel -- O'Connor, Eoin Cornelius -- Luscher, Christian -- England -- Nature. 2014 May 22;509(7501):459-64. doi: 10.1038/nature13257.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Basic Neurosciences, Medical Faculty, University of Geneva, CH-1211 Geneva, Switzerland [2]. ; 1] INSERM, U661, Montpellier F-34094, France [2] CNRS, UMR-5203, Institut de Genomique Fonctionnelle, Montpellier F-34094, France [3] Universites de Montpellier 1 & 2, UMR-5203, Montpellier F-34094, France. ; Department of Basic Neurosciences, Medical Faculty, University of Geneva, CH-1211 Geneva, Switzerland. ; 1] Department of Basic Neurosciences, Medical Faculty, University of Geneva, CH-1211 Geneva, Switzerland [2] Clinic of Neurology, Department of Clinical Neurosciences, Geneva University Hospital, CH-1211 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24848058" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cocaine/*pharmacology ; Cocaine-Related Disorders/pathology/*physiopathology/psychology ; Disease Models, Animal ; Dopaminergic Neurons/drug effects ; Drug-Seeking Behavior/drug effects ; Female ; Hippocampus/cytology/drug effects/pathology ; Male ; Mice ; N-Methylaspartate/metabolism ; Neural Pathways/drug effects ; Neuronal Plasticity/*drug effects ; Nucleus Accumbens/cytology/*drug effects/pathology ; Optogenetics ; Prefrontal Cortex/cytology/drug effects/pathology ; Receptors, AMPA/metabolism ; Receptors, Dopamine D1/metabolism ; Recurrence ; Synapses/drug effects/metabolism ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Cocaine disinhibits dopamine neurons by potentiation of GABA transmission in the ventral tegmental area (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-09-28
    Description: Drug-evoked synaptic plasticity in the mesolimbic system reshapes circuit function and drives drug-adaptive behavior. Much research has focused on excitatory transmission in the ventral tegmental area (VTA) and the nucleus accumbens (NAc). How drug-evoked synaptic plasticity of inhibitory transmission affects circuit adaptations remains unknown. We found that medium spiny neurons expressing dopamine (DA) receptor type 1 (D1R-MSNs) of the NAc project to the VTA, strongly preferring the GABA neurons of the VTA. Repeated in vivo exposure to cocaine evoked synaptic potentiation at this synapse, occluding homosynaptic inhibitory long-term potentiation. The activity of the VTA GABA neurons was thus reduced and DA neurons were disinhibited. Cocaine-evoked potentiation of GABA release from D1R-MSNs affected drug-adaptive behavior, which identifies these neurons as a promising target for novel addiction treatments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bocklisch, Christina -- Pascoli, Vincent -- Wong, Jovi C Y -- House, David R C -- Yvon, Cedric -- de Roo, Mathias -- Tan, Kelly R -- Luscher, Christian -- New York, N.Y. -- Science. 2013 Sep 27;341(6153):1521-5. doi: 10.1126/science.1237059.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Basic Neurosciences, Medical Faculty, University of Geneva, CH-1211 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24072923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cocaine/*pharmacology ; Cocaine-Related Disorders/physiopathology ; Dopaminergic Neurons/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neuronal Plasticity/drug effects ; Synaptic Transmission/drug effects/physiology ; Ventral Tegmental Area/*metabolism ; gamma-Aminobutyric Acid/*drug effects/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    From The Cover: Regulation of a protein phosphatase cascade allows convergent dopamine and glutamate signals to activate ERK in the striatum (2004)
    National Academy of Sciences
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    Publication Date: 2004-12-17
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 5
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    Social transmission of food safety depends on synaptic plasticity in the prefrontal cortex (2019)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2019
    Description: 〈p〉When an animal is facing unfamiliar food, its odor, together with semiochemicals emanating from a conspecific, can constitute a safety message and authorize intake. The piriform cortex (PiC) codes olfactory information, and the inactivation of neurons in the nucleus accumbens (NAc) can acutely trigger consumption. However, the neural circuit and cellular substrate of transition of olfactory perception into value-based actions remain elusive. We detected enhanced activity after social transmission between two mice in neurons of the medial prefrontal cortex (mPFC) that target the NAc and receive projections from the PiC. Exposure to a conspecific potentiated the excitatory postsynaptic currents in NAc projectors, whereas blocking transmission from PiC to mPFC prevented social transmission. Thus, synaptic plasticity in the mPFC is a cellular substrate of social transmission of food safety.〈/p〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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