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Divergent Regulation of Proopiomelanocortin Neurons by Leptin in the Nucleus of the Solitary Tract and in the Arcuate Hypothalamic Nucleus

¹ Department of Medicine, Division of Endocrinology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts
² Department of Psychology and Neuroscience, University of Pennsylvania, Philadelphia, Pennsylvania

Address correspondence and reprint requests to Dr. Christian Bjørbæk, Beth Israel Deaconess Medical Center, Department of Medicine, 330 Brookline Ave., Research North, RN 325, Boston, MA 02215. E-mail: cbjorbae{at}bidmc.harvard.edu; or to Dr. Harvey Grill, University of Pennsylvania, Department of Psychology and Neuroscience, 3720 Walnut St., Philadelphia, PA 19104-6196. E-mail: grill{at}psych.upenn.edu

Proopiomelanocortin (POMC) neurons in the arcuate nucleus (ARC) of the hypothalamus are activated by leptin and mediate part of leptin’s central actions to influence energy balance. However, little is known about potential leptin signaling in POMC neurons located in the nucleus of the solitary tract (NTS), the only other known population of POMC neurons. Leptin-responsive neurons do exist in the NTS, but their neurochemical phenotype is largely unknown. The contribution of NTS POMC neurons versus ARC POMC neurons in leptin action is thus undetermined. We show here that in contrast to POMC neurons in the ARC, leptin does not stimulate phosphorylation of signal-transducer and activator of transcription 3 in NTS POMC neurons of POMC-EGFP reporter mice. In addition, leptin does not induce c-Fos expression in NTS POMC neurons unlike ARC POMC neurons. Fasting induces a fall in POMC mRNA in both the ARC and the NTS, but different from the ARC, the reduction in NTS POMC mRNA is not reversed by leptin. We conclude that POMC neurons in the NTS do not respond to leptin unlike ARC POMC neurons. POMC neurons in the hypothalamus may therefore mediate all of leptin’s signaling via POMC-derived peptides in the central nervous system.

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