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向大鼠孤束核微量注射亚皮摩尔量的神经肽Y(13 - 36)可抵消神经肽Y(1 - 36)和神经肽Y Y1受体激动剂的血管减压反应。

Microinjections of subpicomolar amounts of NPY(13-36) into the nucleus tractus solitarius of the rat counteract the vasodepressor responses of NPY(1-36) and of a NPY Y1 receptor agonist.

作者信息

Yang S N, Narváez J A, Bjelke B, Agnati L F, Fuxe K

机构信息

Department of Histology and Neurobiology, Karolinska Institutet, Stockholm, Sweden.

出版信息

Brain Res. 1993 Sep 3;621(1):126-32. doi: 10.1016/0006-8993(93)90307-9.

Abstract

Microinjections of neuropeptide Y (NPY) (1-36) and of the NPY Y1 agonist [Leu31,Pro34]NPY into the caudal dorsomedial part of the nucleus tractus solitarius (Sol) in the anaesthetized rat led to the development of dose-related vasodepressor and bradycardic responses. The threshold dose of the NPY Y2 agonist NPY(13-36) (50 fmol) significantly counteracted the vasodepressor actions of a close to ED50 dose of NPY(1-36) (2.5 pmol) and of the NPY Y1 agonist (5 pmol). These results indicate that NPY Y1 receptor activation in the Sol leads to the development of a vasodepressor response, which can be counteracted by NPY Y2 receptor activation in the Sol. The results support the existence of a Y2/Y1 receptor-receptor interaction in the Sol, via which NPY Y2 receptors may reduce transduction over NPY Y1 receptors.

摘要

向麻醉大鼠孤束核(Sol)尾端背内侧部分微量注射神经肽Y(NPY)(1-36)和NPY Y1激动剂[Leu31,Pro34]NPY,会导致剂量相关的血管减压和心动过缓反应。NPY Y2激动剂NPY(13-36)(50飞摩尔)的阈剂量显著抵消了接近半数有效剂量的NPY(1-36)(2.5皮摩尔)和NPY Y1激动剂(5皮摩尔)的血管减压作用。这些结果表明,Sol中NPY Y1受体的激活会导致血管减压反应的发生,而Sol中NPY Y2受体的激活可以抵消这种反应。结果支持了Sol中存在Y2/Y1受体-受体相互作用,通过这种相互作用,NPY Y2受体可能会减少NPY Y1受体的信号转导。

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