SEIZURE PROTECTION AND INCREASED NERVE-TERMINAL GABA - DELAYED-EFFECTS OF GABA TRANSAMINASE INHIBITION
SEIZURE PROTECTION AND INCREASED NERVE-TERMINAL GABA - DELAYED-EFFECTS OF GABA TRANSAMINASE INHIBITION
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DOI：
10.1126/science.6768130
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发表时间：
1980-01-01
期刊：
影响因子：
56.9
通讯作者：
IADAROLA, MJ
中科院分区：
文献类型：
--
作者：
GALE, K;IADAROLA, MJ
在大鼠中，通过手术破坏大脑一侧投射到黑质的密集 GABA，评估了存在和不存在含 GABA 的神经末梢时 γ-氨基丁酸 (GABA) 的变化。单次注射γ-乙烯基-GABA（不可逆地抑制GABA转氨酶）后，将去神经黑质的GABA净增加量与完整黑质在不同时间进行比较。总GABA在12小时内达到最大值，但与神经末梢相关的GABA库直到36小时才增加，并在60小时达到峰值。针对最大电击发作的抗惊厥活性的开始和峰值与神经末梢 GABA 增加的时间过程直接平行，但与独立于神经末梢的 GABA 增加的时间进程不呈正相关。这一结果支持这样的观点：神经末梢中 GABA 的升高促进 GABA 介导的突触传递并预测抗惊厥活性。
Changes in γ-aminobutyric acid (GABA) occurring in the presence and in the absence of GABA-containing nerve terminals were estimated in rats in which the dense GABA projection to the substantia nigra was surgically destroyed on one side of the brain. The net increase in GABA of the denervated nigra was compared with that of the intact nigra at various times after a single injection of γ-vinyl-GABA, which irreversibly inhibits GABA transaminase. Total GABA reached a maximum within 12 hours, but the GABA pool associated with nerve terminals did not increase until 36 hours and peaked at 60 hours. The onset and peak of anticonvulsant activity against maximal electroshock seizures directly paralleled the time course for the increase in GABA in nerve terminals, but was not positively correlated with that independent of the terminals. This result supports the concept that elevating GABA in nerve terminals facilitates GABA-mediated synaptic transmission and predicts anticonvulsant activity.