Seizures during ethanol withdrawal are blocked by focal microinjection of excitant amino acid antagonists into the inferior colliculus and pontine reticular formation.
Seizures during ethanol withdrawal are blocked by focal microinjection of excitant amino acid antagonists into the inferior colliculus and pontine reticular formation.
复制标题
通过将兴奋性氨基酸拮抗剂局部显微注射到下丘和脑桥网状结构中，可以阻止乙醇戒断期间的癫痫发作。
DOI：
10.1111/j.1530-0277.1994.tb01450.x
复制
发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Faingold,CL
中科院分区：
文献类型：
--
作者：
Riaz,A;Faingold,CL
对乙醇的身体依赖性可导致乙醇戒断期间癫痫发作的易感性。在大鼠中，酒精戒断综合征期间，听觉刺激可诱发全身强直阵挛性癫痫发作。兴奋性氨基酸（EAA）是下丘和脑干网状结构中的神经递质，在听源性癫痫发作（AGSs）遗传模型的神经网络中发挥重要作用。乙醇会阻断EAA在不同脑区的作用，包括下丘。在这项研究中，通过灌胃乙醇4天产生依赖性。在乙醇戒断期间，通过全身给予竞争性或非竞争性NMDA拮抗剂3-（（±）-2-羧基哌嗪-4-基）-丙基-1-膦酸（CPP）或地佐环平（MK-801）阻断AGSs。向下丘或脑桥网状结构中局灶性显微注射NMDA或非NMDA拮抗剂也可抑制AGSs。MK-801是最有效的全身抗惊厥药。当注射到下丘时，CPP的抗惊厥作用比MK-801或非NMDA拮抗剂6-氰基-7-硝基喹喔啉-2，3-二酮更强。下丘比脑桥网状结构对竞争性NMDA和非NMDA拮抗剂的抗惊厥作用更敏感。目前的结果支持的想法，持续乙醇管理可能会导致发展的超敏反应的行动EAA下丘和脑桥网状结构神经元。这可能是一个关键的机制subserving AGS敏感性在乙醇戒断。
Physical dependence on ethanol can result in seizure susceptibility during ethanol withdrawal. In rats, generalized tonic‐clonic seizures are precipitated by auditory stimulation during the ethanol withdrawal syndrome. Excitant amino acids (EAAs) are implicated as neurotransmitters in the inferior colliculus and the brain stem reticular formation, which play important roles in the neuronal network for genetic models of audiogenicseizures(AGSs). Ethanol blocks the actions of EAAs in various brain regions, including the inferior colliculus. In this study, dependence was produced by intragastric administration of ethanol for 4 days. During ethanol withdrawal, AGSs were blocked by systemic administration of competitive or noncompetitive NMDA antagonists 3‐((±)‐2‐carboxypiperazin‐4‐yl)‐propyl‐1‐phosphonic acid (CPP) or dizocilpine (MK‐801). Focal microinjections of NMDA or non‐NMDA antagonists into the inferior colliculus or the pontine reticular formation also inhibited AGSs. MK‐801 was the most potent anticonvulsant systemically. When injected into the inferior colliculus, CPP had a more potent anticonvulsant effect than either MK‐801 or the non‐NMDA antagonist 6‐cyano‐7‐nitroquinoxa‐line‐2,3‐dione. The inferior colliculus was more sensitive than the pontine reticular formation to the anticonvulsant effects of both competitive NMDA and non‐NMDA antagonists. The results of the present support the idea that continued ethanol administration may lead to development of supersensitivity to the action of EAAs in inferior colliculus and pontine reticular formation neurons. This may be a critical mechanism subserving AGS susceptibility during ethanol withdrawal.