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皮质扩散性抑制对各种惊厥剂诱发的癫痫病灶的不同影响。

Differential effects of cortical speading depression on epileptic foci induced by various convulsants.

作者信息

Ueda M, Bures J

出版信息

Electroencephalogr Clin Neurophysiol. 1977 Nov;43(5):666-74. doi: 10.1016/0013-4694(77)90081-5.

Abstract

Interaction between epileptic foci and spreading depression (SD) was studied in the cerebral cortex of rats anesthetized with Nembutal. At comparable discharge rates, picrotoxin and penicillin caused complete and partial SD blockade respectively, strychnine and Metrazol were ineffective and Aldactone facilitated SD. Conversely, the duration of SD-induced blockade of epileptic activity was maximal for Aldactone and minimal for picrotoxin. Treatment of the picrotoxin focus with tetrodotoxin (10(-4)M) reduced the discharge rate and reinstated SD propagation into the focus. [K+]e measured with ion-selective K+ electrodes 1 mm below the cortical surface increased to 8 mM in penicillin foci blocking SD and remained below 5 mM in Aldactone foci. It is concluded that the differential effect of various convulsants on SD propagation depends on the potassium concentration in the depth of the focus rather than on the discharge rate or on the mechanism of the the epileptogenic effect.

摘要

在使用戊巴比妥麻醉的大鼠大脑皮层中,研究了癫痫病灶与扩散性抑制(SD)之间的相互作用。在可比的放电率下,苦味毒和青霉素分别导致完全和部分SD阻断,士的宁和戊四氮无效,而安体舒通促进SD。相反,SD诱导的癫痫活动阻断持续时间在安体舒通时最长,在苦味毒时最短。用河豚毒素(10^(-4)M)处理苦味毒病灶可降低放电率,并恢复SD向病灶的传播。用离子选择性钾电极在皮层表面以下1毫米处测量的[K+]e在阻断SD的青霉素病灶中增加到8 mM,而在安体舒通病灶中保持在5 mM以下。得出的结论是,各种惊厥剂对SD传播的不同作用取决于病灶深处的钾浓度,而不是放电率或致痫作用机制。

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