Neuropeptide Y, a member of the pancreatic polypeptide family, caused dose-dependent relaxation of guinea pig colon longitudinal muscle. This inhibitory effect was unaffected by hexamethonium but was abolished by atropine and tetrodotoxin, suggesting that neuropeptide Y is acting via postganglionic cholinergic neurons. Studies utilizing alpha-adrenergic and dopamine receptor antagonists revealed that neuropeptide Y-mediated relaxation was blocked only by the alpha 2 antagonist yohimbine. Neuropeptide Y also antagonized muscle response to electric field stimulation that was reversed by yohimbine. Additional studies with muscle slices incubated with [3H]norepinephrine or [3H]choline showed that neuropeptide Y stimulated norepinephrine release from sympathetic nerves, which, in turn, inhibited the release of acetylcholine via alpha 2 receptors located on postganglionic nerves. This pathway provides a mechanism for neuropeptide modulation of classical neurotransmitter function.

译文

神经肽Y是胰多肽家族的成员,引起豚鼠结肠纵向肌的剂量依赖性松弛。这种抑制作用不受六甲铵的影响,但被阿托品和河豚毒素消除,表明神经肽Y通过神经节后胆碱能神经元起作用。利用 α-肾上腺素能和多巴胺受体拮抗剂的研究表明,神经肽Y介导的松弛仅被 α2拮抗剂育亨宾阻断。神经肽Y还拮抗肌肉对电场刺激的反应,育亨宾可以逆转这种反应。用 [3H] 去甲肾上腺素或 [3H] 胆碱孵育的肌肉切片的其他研究表明,神经肽Y刺激了去甲肾上腺素从交感神经的释放,进而,通过位于节后神经上的 α2受体抑制乙酰胆碱的释放,该途径为神经肽调节经典神经递质功能提供了机制。

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