Loss of vesicular zinc and appearance of perikaryal zinc after seizures induced by pilocarpine
Loss of vesicular zinc and appearance of perikaryal zinc after seizures induced by pilocarpine
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DOI：
10.1097/00001756-200105250-00044
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发表时间：
2001-05
期刊：
影响因子：
1.7
通讯作者：
S. Suh;R. Thompson;C. Frederickson
中科院分区：
文献类型：
--
作者：
S. Suh;R. Thompson;C. Frederickson
海人酸（KA）全身给药引起的癫痫持续状态的条件下，导致一个明显的囊泡锌从突触前终末到突触后神经元易位。锌在胞体中的积累已被确定为神经元损伤的一个促成因素。我们在这里表明，另一种形式的癫痫持续状态，引起的毒蕈碱激动剂匹鲁卡品管理，产生锌的变化，基本上是相同的红藻氨酸诱导癫痫发作所产生的。此外，毛果芸香碱癫痫发作后出现锌染色的神经元与显示退行性变化的神经元相同。这一结果表明，锌从突触前扣的损失和锌在突触后胞体的外观可能都发生在癫痫发作本身，无论病因。
The condition of status epilepticus induced by systemic administration of kainic acid (KA) causes an apparent translocation of vesicular zinc from presynaptic boutons into postsynaptic neurons. The accumulation of zinc in the somata has been identified as a contributing cause of neuronal injury. We show here that another form of status epilepticus, induced by administration of the muscarinic agonist pilocarpine, produces changes in zinc that are essentially the same as those produced by the kainic acid-induced seizures. Moreover, neurons that develop zinc staining after pilocarpine seizures are the same that shown degenerative changes. This result suggests that the loss of zinc from presynaptic boutons and the appearance of zinc in postsynaptic somata may both occur in seizures per se, regardless of etiology.