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一氧化氮在延髓中缝核诱发的导水管周围灰质神经元活动抑制中的作用。

Role of nitric oxide in medullary raphe-evoked inhibition of neuronal activity in the periaqueductal gray matter.

作者信息

Lovick T A

机构信息

Department of Physiology, University of Birmingham, U.K.

出版信息

Neuroscience. 1996 Dec;75(4):1203-9. doi: 10.1016/0306-4522(96)00325-9.

DOI:10.1016/0306-4522(96)00325-9
PMID:8938753
Abstract

In male urethane-anaesthetized rats, activation of neurons in nucleus raphe obscurus and the caudal tip of nucleus raphe magnus by microinjection of 50-100 nl 0.1 M D,L-homocysteic acid produced a 75.6 +/- 5.2% reduction in the firing rate in 25 neurons in the lateral and dorsolateral sectors of the periaqueductal gray matter which lasted for 102.3 +/- 13.3s (mean +/- S.E.M.). The duration of the inhibition was significantly reduced in a dose-dependent manner by intracerebroventricular injection of the inhibitor of nitric oxide synthase, N(w)-nitro-L-arginine methyl ester (50-500 micrograms) but not by N(w)-nitro-D-arginine methyl ester (500 micrograms). In contrast, the magnitude of the raphe-evoked inhibition, i.e. the maximum depression of firing rate, was not significantly affected by either isomer. The results suggest that nitric oxide plays a role in the regulation of the excitability of neurons in the midbrain aversive system by the medullary raphe. The selective effect of the nitric oxide synthase inhibitor on the duration, but not the magnitude, of the raphe-evoked inhibition suggests that nitric oxide is not involved in initiating the inhibition. Rather, its role appears to be in maintaining the raphe-evoked inhibition once it has been initiated by a non-nitrergic mechanism.

摘要

在雄性经氨基甲酸乙酯麻醉的大鼠中,通过微量注射50 - 100 nl 0.1 M D,L-高半胱氨酸激活中缝隐核和中缝大核尾端的神经元,可使导水管周围灰质外侧和背外侧区域的25个神经元的放电频率降低75.6 +/- 5.2%,且持续102.3 +/- 13.3秒(平均值 +/- 标准误)。脑室内注射一氧化氮合酶抑制剂N(ω)-硝基-L-精氨酸甲酯(50 - 500微克)可使抑制持续时间以剂量依赖性方式显著缩短,但注射N(ω)-硝基-D-精氨酸甲酯(500微克)则无此作用。相反,中缝诱发的抑制幅度,即放电频率的最大降低程度,不受任何一种异构体的显著影响。结果表明,一氧化氮在延髓中缝对中脑厌恶系统神经元兴奋性的调节中起作用。一氧化氮合酶抑制剂对中缝诱发抑制的持续时间而非幅度具有选择性作用,这表明一氧化氮不参与启动抑制。相反,其作用似乎是在由非一氧化氮能机制启动抑制后维持中缝诱发的抑制。

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