Leptin does not directly affect CNS serotonin neurons to influence appetite |
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| Authors: | Lam Daniel D Leinninger Gina M Louis Gwendolyn W Garfield Alastair S Marston Oliver J Leshan Rebecca L Scheller Erica L Christensen Lyndsay Donato Jose Xia Jing Evans Mark L Elias Carol Dalley Jeffrey W Burdakov Denis I Myers Martin G Heisler Lora K |
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| Affiliation: | 1 Department of Pharmacology, University of Cambridge, Cambridge CB2 1PD, UK;2 Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge CB2 1PD, UK;3 Department of Experimental Psychology, University of Cambridge, Cambridge CB2 1PD, UK;4 Department of Psychiatry, University of Cambridge, Cambridge CB2 1PD, UK;5 Institute of Metabolic Science, University of Cambridge, Cambridge CB2 1PD, UK;6 Division of Metabolism, Endocrinology, and Diabetes, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA;7 School of Dentistry, University of Michigan, Ann Arbor, MI 48109, USA;8 Division of Hypothalamic Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390-9077, USA |
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| Abstract: | Serotonin (5-HT) and leptin play important roles in the modulation of energy balance. Here we investigated mechanisms by which leptin might interact with CNS 5-HT pathways to influence appetite. Although some leptin receptor (LepRb) neurons lie close to 5-HT neurons in the dorsal raphe (DR), 5-HT neurons do not express LepRb. Indeed, while leptin hyperpolarizes some non-5-HT DR neurons, leptin does not alter the activity of DR 5-HT neurons. Furthermore, 5-HT depletion does not impair the anorectic effects of leptin. The serotonin transporter-cre allele (Sert(cre)) is expressed in 5-HT (and developmentally in some non-5-HT) neurons. While Sert(cre) promotes LepRb excision in a few LepRb neurons in the hypothalamus, it is not active in DR LepRb neurons, and neuron-specific Sert(cre)-mediated LepRb inactivation in mice does not alter body weight or adiposity. Thus, leptin does not directly influence 5-HT neurons and does not meaningfully modulate important appetite-related determinants via 5-HT neuron function. |
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