Chen C H, Rogers R C
Department of Biological Sciences, Massachusetts Institute of Technology, Cambridge 02139, USA.
Am J Physiol. 1997 Jul;273(1 Pt 2):R213-8. doi: 10.1152/ajpregu.1997.273.1.R213.
Peptide YY (PYY) is released by endocrine cells in the ileum in response to the presence of fatty acids in the intestinal lumen. Circulating PYY suppresses vagally mediated digestive functions as a consequence of direct action on neurons in the dorsal medulla. Recent evidence from our laboratory suggests that this PYY-mediated inhibition of digestion occurs because of peptide action at the Y2-type receptor in the dorsal medullary region encompassing vago-vagal reflex circuitry. The present study describes the effects of PYY and the specific Y2 agonist peptide PYY-(13-36) on neurons of the dorsal motor nucleus of the vagus (DMN) in both the 1) intact in vivo and 2) in vitro brain stem slice preparation. Our results show that 50% of DMN neurons recorded under in vivo or in vitro conditions, including synaptic blockade, are inhibited by the application of PYY or PYY-(13-36). Approximately 45% are not affected, and only approximately 5% are activated. These results suggest that one of the principal means by which PYY suppresses digestive functions is by the direct inhibition of cholinergic vagal efferent neurons of the DMN via action at a Y2 receptor.
肽YY（PYY）由回肠内分泌细胞释放，以响应肠腔内脂肪酸的存在。循环中的PYY通过直接作用于延髓背侧的神经元，抑制迷走神经介导的消化功能。我们实验室最近的证据表明，这种PYY介导的消化抑制是由于肽作用于延髓背侧区域包含迷走-迷走反射回路的Y2型受体。本研究描述了PYY和特异性Y2激动剂肽PYY-(13 - 36)对迷走神经背运动核（DMN）神经元的影响，实验条件为：1）完整的体内实验；2）体外脑干切片制备。我们的结果显示，在体内或体外条件下记录的DMN神经元中，包括突触阻断情况下，50%的神经元在应用PYY或PYY-(13 - 36)后受到抑制。约45%不受影响，只有约5%被激活。这些结果表明，PYY抑制消化功能的主要方式之一是通过作用于Y2受体直接抑制DMN的胆碱能迷走传出神经元。
