Increased responsiveness of pontine reticular formation neurons associated with audiogenic seizure susceptibility during ethanol withdrawal.
Increased responsiveness of pontine reticular formation neurons associated with audiogenic seizure susceptibility during ethanol withdrawal.
复制标题
乙醇戒断期间与听源性癫痫易感性相关的脑桥网状形成神经元的反应性增加。
DOI：
10.1016/0006-8993(94)90463-4
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发表时间：
1994
期刊：
影响因子：
2.9
通讯作者：
Riaz,A
中科院分区：
文献类型：
--
作者：
Faingold,CL;Riaz,A
在乙醇戒断（ETX）期间观察到对听源性癫痫发作（AGS）的敏感性。脑桥网状结构（PRF）与ETX期间AGS的传播途径有关。本研究探讨了单一的PRF神经元放电模式的变化所产生的乙醇和ETX重复灌胃给药乙醇。将微电极束植入PRF，观察自由活动大鼠的单神经元反应。在初始乙醇给药的动物昏迷，自发和声诱发的PRF神经元放电显着减少。在ETX期间，动物对AGS敏感，并表现出激动和易怒的行为。此时，观察到自发和声诱发的PRF神经元放电显著增加。重复诱导的反应衰减（习惯化）的PRF神经元的反应显着减少，在ETX，导致夸张的声惊吓反应，这可能是AGS的生理基础。先前的报告表明，乙醇增强GABA的作用并降低谷氨酸的作用。在本研究中，在ETX过程中PRF神经元放电增加可能涉及GABAA受体的下调和谷氨酸受体的超敏感性，这可能有助于AGS的易感性。本研究中观察到的PRF神经元放电增加与先前在ETX期间通过PRF显微注射观察到的AGS阻断一致，进一步支持该脑区在乙醇戒断期间AGS传播中的重要作用。
Susceptibility to audiogenic seizures (AGS) is observed during ethanol withdrawal (ETX). The pontine reticular formation (PRF) is implicated in the propagation pathway for AGS during ETX. The present study examined the changes in single PRF neuronal firing patterns produced by ethanol and during ETX following repeated intragastrically administered ethanol. Microwire electrode bundles were implanted into PRF and single neuronal responses in freely moving rats were examined. During initial ethanol administration the animals were stuporous, and spontaneous and acoustically-evoked PRF neuronal firing were reduced significantly. During ETX the animals were susceptible to AGS and displayed agitated and irritable behavior. At this time a significant increase in spontaneous and acoustically-evoked PRF neuronal firing was observed. Repetition-induced response attenuation (habituation) of PRF neuronal responses was significantly diminished during ETX, leading to an exaggerated acoustic startle response, which may be a physiological basis for AGS. Previous reports indicate that ethanol enhances the effects of GABA and decreases the effects of glutamate. The PRF neuronal firing increases during ETX in the present study may involve the down-regulation of GABAAreceptors and supersensitivity of glutamate receptors reported to occur during ETX, which could contribute to AGS susceptibility. The PRF neuronal firing increases observed in the present study in concord with previous observation of AGS blockade by PRF microinjections during ETX further support an important role of this brain region in the propagation of AGS during ethanol withdrawal.