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延髓头端腹外侧通过释放γ-氨基丁酸抑制大鼠孤束核中的反射性心动过缓。

Rostral ventrolateral medulla suppresses reflex bradycardia by the release of gamma-aminobutyric acid in nucleus tractus solitarii of the rat.

作者信息

Len W B, Chan J Y

机构信息

Team of Biomedical Science, Chang-Gung Institute of Nursing, Taoyuan, Taiwan.

出版信息

Synapse. 2001 Jan;39(1):23-31. doi: 10.1002/1098-2396(20010101)39:1<23::AID-SYN4>3.0.CO;2-4.

Abstract

We investigated the role of gamma-aminobutyric acid (GABA) in the nucleus tractus solitarii (NTS), the principal recipient of baroreceptor afferent fibers in the medulla oblongata, in the suppression of cardiac baroreceptor reflex (BRR) response by the rostral ventrolateral medulla (RVLM). Direct microinfusion via reverse microdialysis of L-glutamate (50 microM) into the RVLM promoted an inhibition of the BRR response, alongside an increase in the concentration of GABA in the dialysate collected from the ipsilateral NTS. Such an increase in GABA concentration in the NTS to RVLM activation was site-specific, as microinfusion of L-glutamate into areas outside the confines of RVLM resulted in no discernible change in GABA concentration in the dialysate of the NTS and minimal effect on the cardiac BRR response. The RVLM-induced BRR suppression of cardiac BRR response to microinjection into the bilateral RVLM of L-glutamate (1 nmol) was antagonized by administration into the bilateral NTS of the GABA(A) receptor antagonist, bicuculline methiodide (1 or 5 pmol), or the GABA(B) receptor antagonist, 2-hydroxy-saclofen (100 or 500 pmol). These results suggest that GABA released in the NTS may participate in cardiac BRR suppression induced by glutamatergic activation of the RVLM, via an action on both GABA(A) and GABA(B) receptor subtypes.

摘要

我们研究了γ-氨基丁酸(GABA)在延髓孤束核(NTS)中的作用,NTS是延髓中压力感受器传入纤维的主要接收部位,探讨其在延髓头端腹外侧区(RVLM)抑制心脏压力感受器反射(BRR)反应中的作用。通过反向微透析将L-谷氨酸(50微摩尔)直接微量注入RVLM,可促进BRR反应的抑制,同时从同侧NTS收集的透析液中GABA浓度增加。NTS中GABA浓度因RVLM激活而增加具有位点特异性,因为将L-谷氨酸微量注入RVLM范围以外的区域,导致NTS透析液中GABA浓度无明显变化,且对心脏BRR反应影响极小。向双侧NTS注射GABA(A)受体拮抗剂甲基荷包牡丹碱(1或5皮摩尔)或GABA(B)受体拮抗剂2-羟基-舒洛芬(100或500皮摩尔),可拮抗RVLM诱导的对向双侧RVLM微量注射L-谷氨酸(1纳摩尔)所致的心脏BRR反应抑制。这些结果表明,NTS中释放的GABA可能通过对GABA(A)和GABA(B)受体亚型的作用,参与RVLM谷氨酸能激活诱导的心脏BRR抑制。

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