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印防己毒素惊厥涉及培养的小鼠脊髓神经元上的突触和非突触机制。

Picrotoxin convulsions involve synaptic and nonsynaptic mechanisms on cultured mouse spinal neurons.

作者信息

Barker J L, MacDonald J F

出版信息

Science. 1980 May 30;208(4447):1054-6. doi: 10.1126/science.7375918.

Abstract

The cellular mechanisms underlying picrotoxin-induced convulsive activity were studied by using mouse spinal neurons growing in tissue culture. Picrotoxin-induced convulsive activity in most but not all of the cells studied. The activity could be inverted by polarizing to positive potentials and eliminated either by decreasing the ratio of calcium to magnesium or by applying tetrodotoxin. When applied locally to individual cells, picrotoxin lowered spike threshold and induced spontaneous firing in some but not all cells tested. The results suggest that picrotoxin-induced convulsive activity involves rapidly summating synaptic activity which may be evoked by high-frequency repetitive firing.

摘要

利用在组织培养中生长的小鼠脊髓神经元,研究了印防己毒素诱导惊厥活动的细胞机制。印防己毒素在大多数但并非所有研究的细胞中诱导惊厥活动。通过极化到正电位可使该活动反转,通过降低钙与镁的比例或应用河豚毒素可消除该活动。当局部应用于单个细胞时,印防己毒素降低了动作电位阈值,并在一些但并非所有测试细胞中诱导了自发放电。结果表明,印防己毒素诱导的惊厥活动涉及快速累加的突触活动,这可能由高频重复放电引起。

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