SPECIFIC PETIT MAL ANTICONVULSANTS REDUCE CALCIUM CURRENTS IN THALAMIC NEURONS
SPECIFIC PETIT MAL ANTICONVULSANTS REDUCE CALCIUM CURRENTS IN THALAMIC NEURONS
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DOI：
10.1016/0304-3940(89)90376-5
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发表时间：
1989-03-13
影响因子：
2.5
通讯作者：
PRINCE, DA
中科院分区：
文献类型：
--
作者：
COULTER, DA;HUGUENARD, JR;PRINCE, DA
丘脑神经元的低阈值钙电流（LTCC）在正常丘脑皮质节律的产生中起重要作用，并可能参与癫痫小发作时棘波放电等异常活动的发生。乙琥胺和二甲双酮，抗惊厥药物有效的小，减少LTCC时，应用于丘脑神经元在临床相关浓度。治疗浓度的苯妥英钠和卡马西平，药物无效的控制小发作，对钙电导的影响很小。LTCC减少可能是特异性小发作抗惊厥药抑制棘波活动的重要作用机制。
Low-threshold calcium current (LTCC) in thalamic neurons is important in generation of normal thalamocortical rhythms, and may be involved in the genesis of abnormal activities such as spike-wave discharges that characterize petit mal epilepsy. Ethosuximide and dimethadione, anticonvulsants effective in petit mal, reduced the LTCC when applied to thalamic neurons at clinically relevant concentrations. Therapeutic concentrations of phenytoin and carbamazepine, drugs ineffective in the control of petit mal, had minimal effects on calcium conductances. Reduction in LTCC may be an important mechanism of action by which specific petit mal anticonvulsants depress spike-wave activity.