Itoh M, Ebadi M
Neurochem Res. 1982 Oct;7(10):1287-98. doi: 10.1007/BF00965899.
The intracerebroventricular administration of Zn2+ (0.3 mumol/10 microliters) causes epileptic seizures characterized by running fits, jumping, vocalization, fasiculation of facial muscles, myoclonic movements of the limbs and tonic-clonic convulsions. These episodes are blocked or reversed by gamma-aminobutyric acid (0.4 mumol/10 microliters). When assayed under conditions where pyridoxal phosphate was not added, the activity of glutamic acid decarboxylase decreased significantly in hippocampus from 18.9 to 15.3 and 9.7 mumols 14CO2 formed/gram proteins/20 min, 15 and 30 min following administration of Zn2+. The inhibition of glutamic acid decarboxylase by Zn2+ was selective occurring only in hippocampus and not in the hypothalamus, amygdala, caudate or thalamus. The inhibition of glutamic acid decarboxylase was not due to a reduction in the concentration of endogenous pyridoxal phosphate which remained unaltered in hippocampus following Zn2+ administration.
脑室内注射Zn2+（0.3微摩尔/10微升）会引发癫痫发作，其特征为奔跑发作、跳跃、发声、面部肌肉抽搐、肢体肌阵挛运动以及强直阵挛性惊厥。这些发作可被γ-氨基丁酸（0.4微摩尔/10微升）阻断或逆转。在未添加磷酸吡哆醛的条件下进行测定时，注射Zn2+后15分钟和30分钟，海马体中谷氨酸脱羧酶的活性显著降低，从每克蛋白质每分钟形成18.9微摩尔14CO2降至15.3微摩尔和9.7微摩尔。Zn2+对谷氨酸脱羧酶的抑制具有选择性，仅发生在海马体中，而在下丘脑、杏仁核、尾状核或丘脑中未出现。谷氨酸脱羧酶的抑制并非由于内源性磷酸吡哆醛浓度降低，在注射Zn2+后海马体中该浓度保持不变。
