6-氨甲基-3-甲基-1,4H-1,2,6-苯并噻二嗪-1,1-二氧化物盐酸盐（TAG）的致痫作用：非特异性与特异性抗牛磺酸发病机制
The epileptogenic action of 6-aminomethyl-3-methyl,1-4H-1,2,6-benzothiadiazine-1,1-diazide hydrochloride (TAG): non-specific versus specific antitaurine pathogenesis.
作者信息
Fariello R G, Golden G T, Ente P
出版信息
Brain Res. 1986 Aug 13;380(1):196-200. doi: 10.1016/0006-8993(86)91449-6.
Cortical superfusion with 6-aminomethyl-3-methyl, 1-4H-1,2,6-benzothiadiazine-1,1-diazide hydrocholoride (TAG) at a concentration which selectively blocks taurine (Tau) action fails to modify electroencephalographic (EEG) activity, cortical neuronal firing and caudate-induced inhibition of cortical neuronal activity. Higher concentrations of TAG increase neuronal firing rate and eventually induce EEG interictal spikes that can be suppressed by topical gamma-aminobutyric acid (GABA), but not by glycine or beta-alanine. Topical Tau consistently enhances the epileptiform activity. It is concluded that specific blockade of Tau does not affect any of the physiological function under observation and that the epileptogenic effect of TAG is due to its GABA antagonistic action.
用6-氨甲基-3-甲基-1,4H-1,2,6-苯并噻二嗪-1,1-二氧化物盐酸盐（TAG）进行皮质灌流，其浓度可选择性阻断牛磺酸（Tau）的作用，但未能改变脑电图（EEG）活动、皮质神经元放电以及尾状核诱导的皮质神经元活动抑制。更高浓度的TAG会增加神经元放电率，并最终诱发EEG发作间期棘波，局部应用γ-氨基丁酸（GABA）可抑制这些棘波，但甘氨酸或β-丙氨酸则不能。局部应用Tau可持续增强癫痫样活动。结论是，对Tau的特异性阻断不会影响所观察到的任何生理功能，并且TAG的致癫痫作用归因于其GABA拮抗作用。
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