PYY(3-36) induces Fos in the arcuate nucleus and in both catecholaminergic and non-catecholaminergic neurons in the nucleus tractus solitarius of rats

被引:51
作者
Blevins, J. E. [1 ,2 ]
Chelikani, P. K. [3 ]
Haver, A. C. [4 ]
Reidelberger, R. D. [3 ,4 ]
机构
[1] Univ Washington, Sch Med, Dept Med, Div Metab Endocrinol & Nutr, Seattle, WA USA
[2] VA Puget Sound Hlth Care Syst, Med Res Serv, Seattle, WA 98108 USA
[3] Creighton Univ, Dept Biomed Sci, Omaha, NE 68178 USA
[4] VA Nebraska Western Iowa Hlth Care Syst, Res Serv, Omaha, NE 68105 USA
关键词
PYY(3-36); satiety; forebrain; hindbrain; Fos; tyrosine hydroxylase;
D O I
10.1016/j.peptides.2007.11.003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Peptide YY (3-36) [PYY(3-36)] inhibits feeding in rodents, nonhuman primates and humans, yet the neural circuits underlying this action remain to be determined. Here we assessed whether PYY(3-36) inhibits feeding by activating neurons in forebrain and hindbrain sites containing Y2 receptors and linked to control of food intake, or in hindbrain sites immediately downstream of vagal afferent neurons. Rats received an anorexigenic dose of PYY(3-36), and the number of neurons expressing Fos, an indicator of neuronal activation, was determined in anterior hypothalamus (AH), arcuate nucleus (ARC), dorsomedial hypothalamus (DMH), lateral hypothalamus (LH), ventromedial hypothalamus (VMH), central nucleus of the amygdala (CeA), area postrema (AP), and caudal medial nucleus tractus solitarius (cmNTS), commissural NTS (cNTS), and gelatinosus NTS (gNTS). Expression of tyrosine hydroxylase (TH), an indicator of catecholamine synthesis, was also measured in the cmNTS. PYY(3-36) increased Fos in ARC, cmNTS, gNTS and AP. Approximately 10% of Fos(+) neurons in the cmNTS were TH(+). These results suggest that PYY(3-36) inhibits feeding through direct activation of ARC neurons, and direct and/or indirect activation via vagal afferent nerves of cmNTS, gNTS and AP, including some catecholaminergic neurons in the cmNTS. (C) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:112 / 119
页数:8
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