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大鼠延髓中动脉压力感受器及迷走神经向交感兴奋神经元的传入神经通路

Arterial baroreceptor and vagal inputs to sympathoexcitatory neurons in rat medulla.

作者信息

Sun M K, Guyenet P G

出版信息

Am J Physiol. 1987 Apr;252(4 Pt 2):R699-709. doi: 10.1152/ajpregu.1987.252.4.R699.

Abstract

Lumbar sympathetic nerve discharge and unit activity of reticulospinal sympathoexcitatory (SE) neurons located in nucleus paragigantocellularis lateralis (PGCL) were recorded in rats. The sympathoinhibition produced by low-frequency stimulation of vagal afferents was abolished by bilateral microinjections of 20 pmol of bicuculline methiodide (BIC, a GABA-receptor antagonist) into PGCL and was converted into a pressor response by injections of 100 pmol. These BIC injections also inhibited the arterial baroreflex in a dose-dependent manner. In contrast the sympathoexcitation produced by high-frequency stimulation of vagal afferents was selectively blocked by bilateral injections of kynurenic acid (KYN, a Glu-receptor antagonist) into PGCL. Convergence of vagal excitatory, vagal inhibitory, and arterial baroreceptor inputs was detected in all SE neurons recorded. Single-pulse stimulation of vagal afferents produced up to two peaks of excitation of SE neurons, both blocked by iontophoretic applications of KYN and at least one inhibitory period selectively blocked by iontophoresis of BIC. The results emphasize the importance of SE neurons and surrounding area in integrating the brain vasomotor output to spinal preganglionic neurons.

摘要

在大鼠中记录了腰交感神经放电以及位于外侧巨细胞旁核(PGCL)的网状脊髓交感兴奋(SE)神经元的单位活动。双侧向PGCL微量注射20 pmol的甲磺酸荷包牡丹碱(BIC,一种GABA受体拮抗剂)可消除低频刺激迷走神经传入纤维所产生的交感抑制,而注射100 pmol则可将其转化为升压反应。这些BIC注射还以剂量依赖的方式抑制动脉压力反射。相反,双侧向PGCL注射犬尿氨酸(KYN,一种谷氨酸受体拮抗剂)可选择性阻断高频刺激迷走神经传入纤维所产生的交感兴奋。在所有记录的SE神经元中均检测到迷走神经兴奋性、迷走神经抑制性和动脉压力感受器输入的汇聚。单脉冲刺激迷走神经传入纤维可使SE神经元产生高达两个兴奋峰,两者均被KYN的离子电泳应用所阻断,且至少一个抑制期被BIC的离子电泳选择性阻断。结果强调了SE神经元及其周围区域在整合大脑血管运动输出至脊髓节前神经元方面的重要性。

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