Leptin activates anorexigenic POMC neurons through a neural network in the arcuate nucleus
The administration of leptin to leptin-deficient humans, and the analogous Lepob/Lepob mice, effectively reduces hyperphagia and obesity. But common obesity is associated with elevated leptin, which suggests that obese humans are resistant to this adipocyte hormone. In addition to regulating long-te...
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| Published in | Nature (London) Vol. 411; no. 6836; pp. 480 - 484 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing
24.05.2001
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | The administration of leptin to leptin-deficient humans, and the analogous Lepob/Lepob mice, effectively reduces hyperphagia and obesity. But common obesity is associated with elevated leptin, which suggests that obese humans are resistant to this adipocyte hormone. In addition to regulating long-term energy balance, leptin also rapidly affects neuronal activity. Proopiomelanocortin (POMC) and neuropeptide-Y types of neurons in the arcuate nucleus of the hypothalamus are both principal sites of leptin receptor expression and the source of potent neuropeptide modulators, melanocortins and neuropeptide Y, which exert opposing effects on feeding and metabolism. These neurons are therefore ideal for characterizing leptin action and the mechanism of leptin resistance; however, their diffuse distribution makes them difficult to study. Here we report electrophysiological recordings on POMC neurons, which we identified by targeted expression of green fluorescent protein in transgenic mice. Leptin increases the frequency of action potentials in the anorexigenic POMC neurons by two mechanisms: depolarization through a nonspecific cation channel; and reduced inhibition by local orexigenic neuropeptide-Y/GABA (γ-aminobutyric acid) neurons. Furthermore, we show that melanocortin peptides have an autoinhibitory effect on this circuit. On the basis of our results, we propose an integrated model of leptin action and neuronal architecture in the arcuate nucleus of the hypothalamus. |
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| AbstractList | The administration of leptin to leptin-deficient humans, and the analogous Lep super(ob)/Lep super(ob) mice, effectively reduces hyperphagia and obesity. But common obesity is associated with elevated leptin, which suggests that obese humans are resistant to this adipocyte hormone. In addition to regulating long-term energy balance, leptin also rapidly affects neuronal activity. Proopiomelanocortin (POMC) and neuropeptide-Y types of neurons in the arcuate nucleus of the hypothalamus are both principal sites of leptin receptor expression and the source of potent neuropeptide modulators, melanocortins and neuropeptide Y, which exert opposing effects on feeding and metabolism. These neurons are therefore ideal for characterizing leptin action and the mechanism of leptin resistance; however, their diffuse distribution makes them difficult to study. Here we report electrophysiological recordings on POMC neurons, which we identified by targeted expression of green fluorescent protein in transgenic mice. Leptin increases the frequency of action potentials in the anorexigenic POMC neurons by two mechanisms: depolarization through a nonspecific cation channel; and reduced inhibition by local orexigenic neuropeptide-Y/GABA ( gamma -aminobutyric acid) neurons. Furthermore, we show that melanocortin peptides have an autoinhibitory effect on this circuit. On the basis of our results, we propose an integrated model of leptin action and neuronal architecture in the arcuate nucleus of the hypothalamus. The administration of leptin to leptin-deficient humans, and the analogous Lepob/Lepob mice, effectively reduces hyperphagia and obesity. But common obesity is associated with elevated leptin, which suggests that obese humans are resistant to this adipocyte hormone. In addition to regulating long-term energy balance, leptin also rapidly affects neuronal activity. Proopiomelanocortin (POMC) and neuropeptide-Y types of neurons in the arcuate nucleus of the hypothalamus are both principal sites of leptin receptor expression and the source of potent neuropeptide modulators, melanocortins and neuropeptide Y, which exert opposing effects on feeding and metabolism. These neurons are therefore ideal for characterizing leptin action and the mechanism of leptin resistance; however, their diffuse distribution makes them difficult to study. Here we report electrophysiological recordings on POMC neurons, which we identified by targeted expression of green fluorescent protein in transgenic mice. Leptin increases the frequency of action potentials in the anorexigenic POMC neurons by two mechanisms: depolarization through a nonspecific cation channel; and reduced inhibition by local orexigenic neuropeptide-Y/GABA (γ-aminobutyric acid) neurons. Furthermore, we show that melanocortin peptides have an autoinhibitory effect on this circuit. On the basis of our results, we propose an integrated model of leptin action and neuronal architecture in the arcuate nucleus of the hypothalamus. The administration of leptin to leptin-deficient humans, and the analogous Lep super(ob)/Lep super(ob) mice, effectively reduces hyperphagia and obesity. But common obesity is associated with elevated leptin, which suggests that obese humans are resistant to this adipocyte hormone. In addition to regulating long-term energy balance, leptin also rapidly affects neuronal activity. Proopiomelanocortin (POMC) and neuropeptide-Y types of neurons in the arcuate nucleus of the hypothalamus are both principal sites of leptin receptor expression and the source of potent neuropeptide modulators, melanocortins and neuropeptide Y, which exert opposing effects on feeding and metabolism. These neurons are therefore ideal for characterizing leptin action and the mechanism of leptin resistance; however, their diffuse distribution makes them difficult to study. Here we report electrophysiological recordings on POMC neurons, which we identified by targeted expression of green fluorescent protein in transgenic mice. Leptin increases the frequency of action potentials in the anorexigenic POMC neurons by two mechanisms: depolarization through a nonspecific cation channel; and reduced inhibition by local orexigenic neuropeptide-Y/GABA (g-aminobutyric acid) neurons. Furthermore, we show that melanocortin peptides have an autoinhibitory effect on this circuit. On the basis of our results, we propose an integrated model of leptin action and neuronal architecture in the arcuate nucleus of the hypothalamus. The administration of leptin to leptin-deficient humans, and the analogous Lepob /Lepob mice, effectively reduces hyperphagia and obesity. But common obesity is associated with elevated leptin, which suggests that obese humans are resistant to this adipocyte hormone. In addition to regulating long-term energy balance, leptin also rapidly affects neuronal activity. Proopiomelanocortin (POMC) and neuropeptide-Y types of neurons in the arcuate nucleus of the hypothalamus are both principal sites of leptin receptor expression and the source of potent neuropeptide modulators, melanocortins and neuropeptide Y, which exert opposing effects on feeding and metabolism. These neurons are therefore ideal for characterizing leptin action and the mechanism of leptin resistance; however, their diffuse distribution makes them difficult to study. Here we report electrophysiological recordings on POMC neurons, which we identified by targeted expression of green fluorescent protein in transgenic mice. Leptin increases the frequency of action potentials in the anorexigenic POMC neurons by two mechanisms: depolarization through a nonspecific cation channel; and reduced inhibition by local orexigenic neuropeptide-Y/GABA (-aminobutyric acid) neurons. Furthermore, we show that melanocortin peptides have an autoinhibitory effect on this circuit. On the basis of our results, we propose an integrated model of leptin action and neuronal architecture in the arcuate nucleus of the hypothalamus. The administration of leptin to leptin-deficient humans, and the analogous Lep(ob)/Lep(ob) mice, effectively reduced hyperphagia and obesity. But commone obesity is associated with elevated leptin, which suggests that obese humans are resistant to this adipocyte hormone. The administration of leptin to leptin-deficient humans, and the analogous Lepob/Lepob mice, effectively reduces hyperphagia and obesity. But common obesity is associated with elevated leptin, which suggests that obese humans are resistant to this adipocyte hormone. In addition to regulating long-term energy balance, leptin also rapidly affects neuronal activity. Proopiomelanocortin (POMC) and neuropeptide-Y types of neurons in the arcuate nucleus of the hypothalamus are both principal sites of leptin receptor expression and the source of potent neuropeptide modulators, melanocortins and neuropeptide Y, which exert opposing effects on feeding and metabolism. These neurons are therefore ideal for characterizing leptin action and the mechanism of leptin resistance; however, their diffuse distribution makes them difficult to study. Here we report electrophysiological recordings on POMC neurons, which we identified by targeted expression of green fluorescent protein in transgenic mice. Leptin increases the frequency of action potentials in the anorexigenic POMC neurons by two mechanisms: depolarization through a nonspecific cation channel; and reduced inhibition by local orexigenic neuropeptide-Y/GABA (gamma-aminobutyric acid) neurons. Furthermore, we show that melanocortin peptides have an autoinhibitory effect on this circuit. On the basis of our results, we propose an integrated model of leptin action and neuronal architecture in the arcuate nucleus of the hypothalamus. |
| Audience | Academic |
| Author | Horvath, Tamas L Rubinstein, Marcelo Cerdán, Marcelo G Cone, Roger D Low, Malcolm J Cowley, Michael A Smart, James L Diano, Sabrina |
| Author_xml | – givenname: Sabrina surname: Diano fullname: Diano, Sabrina organization: Reproductive Neurosciences Unit, Department of Obstetrics and Gynecology – givenname: Tamas L surname: Horvath fullname: Horvath, Tamas L organization: Reproductive Neurosciences Unit, Department of Obstetrics and Gynecology Department of Neurobiology, Yale Medical School – givenname: James L surname: Smart fullname: Smart, James L organization: The Vollum Institute, Oregon Health Sciences University – givenname: Michael A surname: Cowley fullname: Cowley, Michael A organization: The Vollum Institute, Oregon Health Sciences University – givenname: Roger D surname: Cone fullname: Cone, Roger D organization: The Vollum Institute, Oregon Health Sciences University – givenname: Malcolm J surname: Low fullname: Low, Malcolm J organization: The Vollum Institute, Oregon Health Sciences University – givenname: Marcelo surname: Rubinstein fullname: Rubinstein, Marcelo organization: Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, CONICET and Department of Biology, School of Sciences, University of Buenos Aires – givenname: Marcelo G surname: Cerdán fullname: Cerdán, Marcelo G organization: Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, CONICET and Department of Biology, School of Sciences, University of Buenos Aires |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=980127$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/11373681$$D View this record in MEDLINE/PubMed |
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| CODEN | NATUAS |
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| Snippet | The administration of leptin to leptin-deficient humans, and the analogous Lepob/Lepob mice, effectively reduces hyperphagia and obesity. But common obesity is... The administration of leptin to leptin-deficient humans, and the analogous Lep(ob)/Lep(ob) mice, effectively reduced hyperphagia and obesity. But commone... The administration of leptin to leptin-deficient humans, and the analogous Lep super(ob)/Lep super(ob) mice, effectively reduces hyperphagia and obesity. But... The administration of leptin to leptin-deficient humans, and the analogous Lepob /Lepob mice, effectively reduces hyperphagia and obesity. But common obesity... |
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| SubjectTerms | Action Potentials Animals Animals, Genetically Modified Anorexia Arcuate Nucleus of Hypothalamus - physiology Biological and medical sciences Electrophysiology Energy balance Evoked Potentials Fundamental and applied biological sciences. Psychology gamma-Aminobutyric Acid - metabolism Green Fluorescent Proteins Hormones Hormones and neuropeptides. Regulation Hypothalamus. Hypophysis. Epiphysis. Urophysis Leptin - physiology Luminescent Proteins - genetics Male Mice Mice, Inbred C57BL Nerve Net - physiology Neural Inhibition Neural networks Neurons Neurons - physiology Neuropeptide Y - metabolism Obesity Peptides Pro-Opiomelanocortin - physiology Vertebrates: endocrinology |
| Title | Leptin activates anorexigenic POMC neurons through a neural network in the arcuate nucleus |
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