PYY in brain stem nuclei induces vagal stimulation of gastric acid secretion in rats.

PYY in brain stem nuclei induces vagal stimulation of gastric acid secretion in rats.
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脑干核中的 PYY 诱导大鼠迷走神经刺激胃酸分泌。

DOI:
10.1152/ajpgi.1995.268.6.g943
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发表时间:
1995
期刊:
The American journal of physiology.
影响因子:
--
通讯作者:
Tache,Y
Tache,Y
中科院分区:
--
文献类型:
--
作者:
Yang,H;Tache,Y

文献摘要

被引文献

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在带有胃插管的尿烷麻醉大鼠中研究了显微注射到脑干核中的肽 YY (PYY) 对胃酸分泌 (GAS) 的影响。将 PYY (30-200 ng) 显微注射到迷走神经背侧运动核 (DMN) 中,可诱导剂量相关且迷走神经依赖性的 GAS 刺激(从 13 +/- 4 微摩尔/90 分钟净增加至 59 +/- 12 微摩尔/90 分钟)。 PYY (200 ng) 静脉内注射到 DMN 附近的部位没有效果。通过共注射促甲状腺激素释放激素(TRH,30 ng)或血清素受体(5-HT2)激动剂(+/-)-1-(4-甲基-1-哌嗪基)-吡咯并(1,2-a)喹喔啉(357 ng)以及将红藻氨酸(1 ng)微量注射到中缝中,可增强 PYY 诱导进入 DMN 的 GAS苍白球。 Prepro-TRH-(160-169)(200 ng 加入 DMN)不影响 PYY 的刺激作用。将 PYY (200 ng) 显微注射到苍白中缝、暗中缝和模糊核中也增加了 GAS,尽管反应持续时间比 DMN 中的要短。这些结果表明,PYY 在涉及 GAS 迷走神经调节的脑干核中起作用,并且 PYY 在 DMN 中的作用被作用于该位点的 TRH 或 5-HT2 受体激动剂增强。
The influence of peptide YY (PYY) microinjected into brain stem nuclei on gastric acid secretion (GAS) was investigated in urethan-anesthetized rats with gastric cannula. PYY (30-200 ng) microinjected into the dorsal motor nucleus of the vagus (DMN) induces a dose-related and vagal-dependent stimulation of GAS (net increase from 13 +/- 4 to 59 +/- 12 mumol/90 min). PYY (200 ng) injected intravenously intracisternally into sites adjacent to the DMN had no effect. GAS induced by PYY into the DMN was potentiated by coinjection of thyrotropin-releasing hormone (TRH, 30 ng) or the serotonin receptor (5-HT2) agonist (+/-)-1-(4-methyl-1-piperazinyl)-pyrrolo(1,2-a)quinoxaline (357 ng) and by microinjection of kainic acid (1 ng) into the raphe pallidus. Prepro-TRH-(160-169) (200 ng into the DMN) did not influence the stimulatory effect of PYY. PYY (200 ng) microinjected into the raphe pallidus, raphe obscurus, and nucleus ambiguous also increased GAS, although the response was of shorter duration than that in the DMN. These results indicate that PYY acts in brain stem nuclei involved in the vagal regulation of GAS and that PYY action in the DMN is potentiated by TRH or 5-HT2 receptor agonist acting at this site.