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Cell Metab. 2017 Feb 7;25(2):322-334. doi: 10.1016/j.cmet.2016.12.002. Epub 2017 Jan 5.

Medullary Reticular Neurons Mediate Neuropeptide Y-Induced Metabolic Inhibition and Mastication.

Author information

  • 1Department of Integrative Physiology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
  • 2Department of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine, Maebashi 371-8511, Japan.
  • 3Department of Neurological Surgery, Oregon Health & Science University, Portland, OR 97239, USA.
  • 4Department of Integrative Physiology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan; PRESTO, Japan Science and Technology Agency, Kawaguchi, Saitama 332-0012, Japan. Electronic address: kazu@med.nagoya-u.ac.jp.

Abstract

Hypothalamic neuropeptide Y (NPY) elicits hunger responses to increase the chances of surviving starvation: an inhibition of metabolism and an increase in feeding. Here we elucidate a key central circuit mechanism through which hypothalamic NPY signals drive these hunger responses. GABAergic neurons in the intermediate and parvicellular reticular nuclei (IRt/PCRt) of the medulla oblongata, which are activated by NPY-triggered neural signaling from the hypothalamus, potentially through the nucleus tractus solitarius, mediate the NPY-induced inhibition of metabolic thermogenesis in brown adipose tissue (BAT) via their innervation of BAT sympathetic premotor neurons. Intriguingly, the GABAergic IRt/PCRt neurons innervating the BAT sympathetic premotor region also innervate the masticatory motor region, and stimulation of the IRt/PCRt elicits mastication and increases feeding as well as inhibits BAT thermogenesis. These results indicate that GABAergic IRt/PCRt neurons mediate hypothalamus-derived hunger signaling by coordinating both autonomic and feeding motor systems to reduce energy expenditure and to promote feeding.

KEYWORDS:

brown adipose tissue; cardiovascular; feeding; hunger; medulla; metabolism; neural circuit; obesity; sympathetic; thermoregulation

PMID:
28065829
PMCID:
PMC5299028
[Available on 2018-02-07]
DOI:
10.1016/j.cmet.2016.12.002
[PubMed - in process]
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