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  • 1
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    UCP2 mediates ghrelin's action on NPY/AgRP neurons by lowering free radicals (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-08-01
    Description: The gut-derived hormone ghrelin exerts its effect on the brain by regulating neuronal activity. Ghrelin-induced feeding behaviour is controlled by arcuate nucleus neurons that co-express neuropeptide Y and agouti-related protein (NPY/AgRP neurons). However, the intracellular mechanisms triggered by ghrelin to alter NPY/AgRP neuronal activity are poorly understood. Here we show that ghrelin initiates robust changes in hypothalamic mitochondrial respiration in mice that are dependent on uncoupling protein 2 (UCP2). Activation of this mitochondrial mechanism is critical for ghrelin-induced mitochondrial proliferation and electric activation of NPY/AgRP neurons, for ghrelin-triggered synaptic plasticity of pro-opiomelanocortin-expressing neurons, and for ghrelin-induced food intake. The UCP2-dependent action of ghrelin on NPY/AgRP neurons is driven by a hypothalamic fatty acid oxidation pathway involving AMPK, CPT1 and free radicals that are scavenged by UCP2. These results reveal a signalling modality connecting mitochondria-mediated effects of G-protein-coupled receptors on neuronal function and associated behaviour.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4101536/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4101536/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andrews, Zane B -- Liu, Zhong-Wu -- Walllingford, Nicholas -- Erion, Derek M -- Borok, Erzsebet -- Friedman, Jeffery M -- Tschop, Matthias H -- Shanabrough, Marya -- Cline, Gary -- Shulman, Gerald I -- Coppola, Anna -- Gao, Xiao-Bing -- Horvath, Tamas L -- Diano, Sabrina -- R01 AG022880/AG/NIA NIH HHS/ -- R01 DK040936/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Aug 14;454(7206):846-51. doi: 10.1038/nature07181. Epub 2008 Jul 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Comparative Medicine, Department of Obstetrics, Gynecology & Reproductive Sciences, Howard Hughes Medical Institute, New York, New York 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18668043" target="_blank"〉PubMed〈/a〉
    Keywords: Agouti-Related Protein/genetics/*metabolism ; Animals ; Carnitine O-Palmitoyltransferase/metabolism ; Fatty Acids/metabolism ; Feeding Behavior/drug effects ; Gene Expression Regulation/drug effects ; Ghrelin/*metabolism/pharmacology ; Hypothalamus/drug effects/metabolism ; Ion Channels/genetics/*metabolism ; Membrane Potential, Mitochondrial/drug effects/physiology ; Mice ; Mitochondria/drug effects/physiology ; Mitochondrial Proteins/genetics/*metabolism ; Neurons/drug effects/*metabolism ; Neuropeptide Y/genetics/*metabolism ; Phosphorylation/drug effects ; Reactive Oxygen Species/*metabolism ; Synapses/drug effects/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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  • 2
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    Rapid regulation of depression-related behaviours by control of midbrain dopamine neurons (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-12-14
    Description: Ventral tegmental area (VTA) dopamine neurons in the brain's reward circuit have a crucial role in mediating stress responses, including determining susceptibility versus resilience to social-stress-induced behavioural abnormalities. VTA dopamine neurons show two in vivo patterns of firing: low frequency tonic firing and high frequency phasic firing. Phasic firing of the neurons, which is well known to encode reward signals, is upregulated by repeated social-defeat stress, a highly validated mouse model of depression. Surprisingly, this pathophysiological effect is seen in susceptible mice only, with no apparent change in firing rate in resilient individuals. However, direct evidence--in real time--linking dopamine neuron phasic firing in promoting the susceptible (depression-like) phenotype is lacking. Here we took advantage of the temporal precision and cell-type and projection-pathway specificity of optogenetics to show that enhanced phasic firing of these neurons mediates susceptibility to social-defeat stress in freely behaving mice. We show that optogenetic induction of phasic, but not tonic, firing in VTA dopamine neurons of mice undergoing a subthreshold social-defeat paradigm rapidly induced a susceptible phenotype as measured by social avoidance and decreased sucrose preference. Optogenetic phasic stimulation of these neurons also quickly induced a susceptible phenotype in previously resilient mice that had been subjected to repeated social-defeat stress. Furthermore, we show differences in projection-pathway specificity in promoting stress susceptibility: phasic activation of VTA neurons projecting to the nucleus accumbens (NAc), but not to the medial prefrontal cortex (mPFC), induced susceptibility to social-defeat stress. Conversely, optogenetic inhibition of the VTA-NAc projection induced resilience, whereas inhibition of the VTA-mPFC projection promoted susceptibility. Overall, these studies reveal novel firing-pattern- and neural-circuit-specific mechanisms of depression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3554860/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3554860/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chaudhury, Dipesh -- Walsh, Jessica J -- Friedman, Allyson K -- Juarez, Barbara -- Ku, Stacy M -- Koo, Ja Wook -- Ferguson, Deveroux -- Tsai, Hsing-Chen -- Pomeranz, Lisa -- Christoffel, Daniel J -- Nectow, Alexander R -- Ekstrand, Mats -- Domingos, Ana -- Mazei-Robison, Michelle S -- Mouzon, Ezekiell -- Lobo, Mary Kay -- Neve, Rachael L -- Friedman, Jeffrey M -- Russo, Scott J -- Deisseroth, Karl -- Nestler, Eric J -- Han, Ming-Hu -- F31 MH095425/MH/NIMH NIH HHS/ -- F32 MH096464/MH/NIMH NIH HHS/ -- K99 MH094405/MH/NIMH NIH HHS/ -- R01 MH092306/MH/NIMH NIH HHS/ -- R25 GM064118/GM/NIGMS NIH HHS/ -- T32 MH020016/MH/NIMH NIH HHS/ -- T32 MH087004/MH/NIMH NIH HHS/ -- T32 MH096678/MH/NIMH NIH HHS/ -- England -- Nature. 2013 Jan 24;493(7433):532-6. doi: 10.1038/nature11713. Epub 2012 Dec 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Systems Therapeutics, Friedman Brain Institute, Mount Sinai School of Medicine, New York, New York 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23235832" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Depression/etiology/*physiopathology ; Dopaminergic Neurons/*metabolism ; Food Preferences ; Male ; Mesencephalon/*cytology ; Mice ; Neural Pathways ; Nucleus Accumbens/physiology ; Optogenetics ; Phenotype ; Prefrontal Cortex/physiology ; *Social Behavior ; Stress, Psychological/complications/*physiopathology ; Sucrose/administration & dosage ; Time Factors ; Ventral Tegmental Area/physiology
    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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    Bidirectional electromagnetic control of the hypothalamus regulates feeding and metabolism (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-03-24
    Description: Targeted, temporally regulated neural modulation is invaluable in determining the physiological roles of specific neural populations or circuits. Here we describe a system for non-invasive, temporal activation or inhibition of neuronal activity in vivo and its use to study central nervous system control of glucose homeostasis and feeding in mice. We are able to induce neuronal activation remotely using radio waves or magnetic fields via Cre-dependent expression of a GFP-tagged ferritin fusion protein tethered to the cation-conducting transient receptor potential vanilloid 1 (TRPV1) by a camelid anti-GFP antibody (anti-GFP-TRPV1). Neuronal inhibition via the same stimuli is achieved by mutating the TRPV1 pore, rendering the channel chloride-permeable. These constructs were targeted to glucose-sensing neurons in the ventromedial hypothalamus in glucokinase-Cre mice, which express Cre in glucose-sensing neurons. Acute activation of glucose-sensing neurons in this region increases plasma glucose and glucagon, lowers insulin levels and stimulates feeding, while inhibition reduces blood glucose, raises insulin levels and suppresses feeding. These results suggest that pancreatic hormones function as an effector mechanism of central nervous system circuits controlling blood glucose and behaviour. The method we employ obviates the need for permanent implants and could potentially be applied to study other neural processes or used to regulate other, even dispersed, cell types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stanley, Sarah A -- Kelly, Leah -- Latcha, Kaamashri N -- Schmidt, Sarah F -- Yu, Xiaofei -- Nectow, Alexander R -- Sauer, Jeremy -- Dyke, Jonathan P -- Dordick, Jonathan S -- Friedman, Jeffrey M -- GM067545/GM/NIGMS NIH HHS/ -- GM095654/GM/NIGMS NIH HHS/ -- MH105941/MH/NIMH NIH HHS/ -- U01 MH105941/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Mar 31;531(7596):647-50. doi: 10.1038/nature17183. Epub 2016 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics, Rockefeller University, New York, New York 10065, USA. ; Department of Chemical &Biological Engineering, Center for Biotechnology &Interdisciplinary Studies, Rensselaer Polytechnic Institute, Troy, New York 12180, USA. ; Department of Radiology, Weill Cornell Medical College, New York, New York 10065, USA. ; Howard Hughes Medical Institute, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27007848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/*metabolism ; Eating/*physiology ; Ferritins/genetics/metabolism ; Glucagon/blood ; Glucokinase/metabolism ; Homeostasis ; Hypoglycemia/metabolism ; Insulin/blood ; Integrases/metabolism ; *Magnetic Fields ; Mice ; Neural Inhibition ; Neurons/*physiology ; Pancreatic Hormones/metabolism ; *Radio Waves ; Recombinant Fusion Proteins/genetics/metabolism ; TRPV Cation Channels/genetics/metabolism ; Time Factors ; Ventromedial Hypothalamic Nucleus/*cytology/*physiology
    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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