[NMDA受体拮抗剂MK-801脑血管效应的γ-氨基丁酸能机制]
[GABAergic mechanism of cerebrovascular effect of the NMDA receptor antagonist MK-801].
作者信息
Gan'shina T S, Gnezdilova A V, Kurza E V, Turilova A I, Mirzoian R S
出版信息
Eksp Klin Farmakol. 2014;77(6):8-12.
PMID:25102728
Abstract
NMDA receptor antagonist MK-801 (dizocilpine) increases the local blood flow in the cerebral cortex in rats under transient global ischemia (TGI) conditions to a greater degree than in intact animals. The GABA receptor blocker bicuculline in most experiments eliminates or reduces the MK-801 induced increase in the blood flow after TGI, which is indicative of the participation of GABAergic mechanism of cerebrovascular tone control in the observed MK-801 activity.
摘要
N-甲基-D-天冬氨酸（NMDA）受体拮抗剂MK-801（地佐环平）在短暂性全脑缺血（TGI）条件下比在正常动物中更大程度地增加大鼠大脑皮质的局部血流量。在大多数实验中，GABA受体阻断剂荷包牡丹碱消除或降低了TGI后MK-801诱导的血流量增加，这表明脑血管张力控制的GABA能机制参与了所观察到的MK-801活性。
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