...
首页> 外文期刊>The European Journal of Neuroscience >Hypocretin-1 causes G protein activation and increases ACh release in rat pons.
【24h】

Hypocretin-1 causes G protein activation and increases ACh release in rat pons.

机译:Hypocretin-1导致G蛋白激活并增加大鼠脑桥中ACh的释放。

获取原文
获取原文并翻译 | 示例
           

摘要

The effects of the arousal-promoting peptide hypocretin on brain stem G protein activation and ACh release were examined using 16 adult Sprague-Dawley rats. In vitro[35S]GTPgammaS autoradiography was used to test the hypothesis that hypocretin-1-stimulated G protein activation is concentration-dependent and blocked by the hypocretin receptor antagonist SB-334867. Activated G proteins were quantified in dorsal raphe nucleus (DR), locus coeruleus (LC) and pontine reticular nucleus oral part (PnO) and caudal part (PnC). Concentration-response data revealed a significant (P < 0.001) effect of hypocretin-1 (2-2000 nm) in all brain regions examined. Maximal increases over control levels of [35S]GTPgammaS binding were 37% (DR), 58% (LC), 52% (PnO) and 44% (PnC). SB-334867 (2 micro m) significantly (P < 0.002) blocked hypocretin-1 (200 nm)-stimulated [35S]GTPgammaS binding in all four nuclei. This is the first autoradiographic demonstration that hypocretin-1 activates G proteins in arousal-related brain stem nuclei as a result of specific receptor interactions. This finding suggests that some hypocretin receptors in brain stem couple to inhibitory G proteins. In vivo microdialysis was used to test the hypothesis that PnO administration of hypocretin-1 increases ACh release in PnO. Dialysis delivery of hypocretin-1 (100 micro m) significantly (P < 0.002) increased (87%) ACh release. This finding is consistent with the interpretation that one mechanism by which hypocretin promotes arousal is by enhancing cholinergic neurotransmission in the pontine reticular formation.
机译:使用16只成年Sprague-Dawley大鼠,研究了促进刺激的肽降钙素对脑干G蛋白活化和ACh释放的影响。体外[35S] GTPgammaS放射自显影技术用于检验以下假设的假设:降钙素-1刺激的G蛋白活化是浓度依赖性的,并被降钙素受体拮抗剂SB-334867阻断。活化的G蛋白定量在背缝核(DR),蓝斑轨迹(LC)和桥脑网状核口腔部分(PnO)和尾部(PnC)中。浓度反应数据显示,在所有检查的大脑区域中,hypocretin-1(2-2000 nm)均具有显着(P <0.001)作用。 [35S] GTPgammaS结合的对照水平的最大增加为37%(DR),58%(LC),52%(PnO)和44%(PnC)。 SB-334867(2微米)显着(P <0.002)阻断了hypocretin-1(200 nm)刺激的所有四个核中的[35S] GTPgammaS结合。这是放射自显影的首次证明,由于特定的受体相互作用,hypocretin-1激活了与觉醒相关的脑干核中的G蛋白。这一发现表明脑干中的一些降钙素受体与抑制性G蛋白偶联。体内微透析用于测试以下假设,即PnO给予hypocretin-1会增加PnO中ACh的释放。降钙素1(100微米)的透析递送显着(P <0.002)增加(87%)ACh释放。该发现与以下解释相符,即促胰降血糖素促进唤醒的一种机制是通过增强桥脑网状结构中的胆碱能神经传递。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号