Role of TRPV1 in susceptibility to PTZ-induced seizure following repeated hyperthermia challenges in neonatal mice

Role of TRPV1 in susceptibility to PTZ-induced seizure following repeated hyperthermia challenges in neonatal mice
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TRPV1 在新生小鼠反复高温挑战后对 PTZ 诱导癫痫发作易感性中的作用

DOI:
10.1016/j.yebeh.2013.10.022
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发表时间:
2014-02-01
影响因子:
2.6
通讯作者:
Peng, Bi-Wen
Peng, Bi-Wen
中科院分区:
医学3区
文献类型:
--
作者:
Kong, Wei-Lin;Min, Jia-Wei;Peng, Bi-Wen

文献摘要

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本研究旨在探讨实验性热性惊厥在全身阵挛性惊厥中的作用及热敏通道TRPV 1的参与。使用戊四氮诱导的阵挛性癫痫发作作为癫痫发作模型,使用Trpv 1基因敲除和野生型C57/BL 6小鼠作为实验对象。记录脑电图和癫痫发作行为,以评估癫痫发作的严重程度。实验性热性惊厥频率增加促进PTZ诱导的全身阵挛性惊厥发作。trpv 1基因缺陷降低了全身性阵挛发作的性质。实验性热性惊厥的强度降低了全身性阵挛性癫痫发作的阈值,Trpv 1基因缺陷降低了小鼠早期高温挑战后对PTZ诱导癫痫发作的易感性。(C)2013 Elsevier Inc. All rights reserved.
This study was designed to investigate the role of experimental febrile seizures in the induction of generalized clonic seizures and the involvement of heat-sensitive channel TRPV1. Pentylenetetrazol-induced clonic seizure was used as the seizure model, and Trpv1 gene knock-out and wild-type C57/BL6 mice were used as experimental subjects. Electroencephalograph and seizure behavior were recorded for the evaluation of the severity of seizures. Increased frequency of the experimental febrile seizures facilitated PTZ-induced generalized clonic seizures. Trpv1 gene deficiency decreased the properties of generalized clonic seizure. The intensity of experimental febrile seizures reduced the threshold to generalized clonic seizure, and Trpv1 gene deficiency decreased the susceptibility to PTZ-induced seizures following early-life hyperthermia challenges in mice. (C) 2013 Elsevier Inc. All rights reserved.