Ostrovskaia R U, Molodavkin G M
Biull Eksp Biol Med. 1978 Aug;86(8):192-4.
Screening and electrophysiological methods were applied to the verification of the hypothesis on a possibility of participation of cholinergic structures in the realization of bicucullin effects. M- and N-cholinolytics (benactizine, atropine, aprophen, and pediphen) failed to arrest the convulsions induced in mice by bicucullin adminstration. At the same time substances inducing accumulation of gamma-aminobutyric acid (GABA) in the brain, i.e. aminooxycetic acid and depakin produced a manifest protective action in convulsions caused by bicucullin administration. In electrophysiological experiments there was also revealed an incapacity of M-cholinolytic benaltizine to arrest the bicucullin effects. Bicucullin proved to diminish depression of the test response in the restoration cycle of the primary response of the rat sensory motor cortex at the intervals of 40--125ms between the stimuli, whereas benactizine decreased the late facilitation of the test response at the intervals of 150--300ms between the stimuli. There was also noted no interaction between benactizine and bicucullin by this test. On the basis of these data a conclusion was drawn that bicucullin effects were caused by the block of postsynaptic GABA receptors, and were not connected with the cholinergic structures activity.
采用筛选和电生理方法来验证关于胆碱能结构参与荷包牡丹碱效应实现可能性的假说。M型和N型胆碱能阻断剂（苯乃嗪、阿托品、阿普罗芬和苯海拉明）未能阻止因给予荷包牡丹碱而在小鼠中诱发的惊厥。与此同时，能诱导大脑中γ-氨基丁酸（GABA）积累的物质，即氨氧乙酸和丙戊酸钠，在因给予荷包牡丹碱而引起的惊厥中产生了明显的保护作用。在电生理实验中还发现，M型胆碱能阻断剂苯乃嗪无法阻止荷包牡丹碱的效应。事实证明，荷包牡丹碱会在刺激间隔为40 - 125毫秒时降低大鼠感觉运动皮层初级反应恢复周期中测试反应的抑制，而苯乃嗪则会在刺激间隔为150 - 300毫秒时降低测试反应的晚期易化。通过该测试还未发现苯乃嗪与荷包牡丹碱之间存在相互作用。基于这些数据得出结论，荷包牡丹碱的效应是由突触后GABA受体的阻断引起的，与胆碱能结构的活性无关。
