Increased Susceptibility to Pilocarpine-Induced Status Epilepticus and Reduced Latency in TRPC1/4 Double Knockout Mice.
Increased Susceptibility to Pilocarpine-Induced Status Epilepticus and Reduced Latency in TRPC1/4 Double Knockout Mice.
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DOI：
10.3390/neurolint15040095
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发表时间：
2023-12-06
影响因子：
3
通讯作者：
Shwe UT
中科院分区：
文献类型：
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作者：
Zheng F;Phelan KD;Shwe UT
典型瞬时受体电位通道(TRPC)是一类钙离子通透性阳离子通道。以往的研究表明，由TRPC1和TRPC4组成的异构体通道在外侧隔神经元和海马CA1区锥体神经元中介导癫痫样放电，提示TRPC1/4通道具有致痫作用。在这项研究中，我们利用脑电记录和频谱分析来评估TRPC1/4通道在匹罗卡品癫痫持续状态(SE)模型中的作用。我们发现，令人惊讶的是，TRPC1/4双基因敲除(DKO)小鼠对匹罗卡品诱导的SE的易感性增加。此外，TRPC1/4 DKO小鼠的SE潜伏期也显著缩短。需要进一步的研究来揭示我们意想不到的结果的潜在机制。
Canonical transient receptor potential channels (TRPCs) are a family of calcium-permeable cation channels. Previous studies have shown that heteromeric channels comprising TRPC1 and TRPC4 mediate epileptiform bursting in lateral septal neurons and hippocampal CA1 pyramidal neurons, suggesting that TRPC1/4 channels play a pro-seizure role. In this study, we utilized electroencephalography (EEG) recording and spectral analysis to assess the role of TRPC1/4 channels in the pilocarpine model of status epilepticus (SE). We found that, surprisingly, TRPC1/4 double knockout (DKO) mice exhibited an increased susceptibility to pilocarpine-induced SE. Furthermore, SE latency was also significantly reduced in TRPC1/4 DKO mice. Further studies are needed to reveal the underlying mechanisms of our unexpected results.
影响因子：
4.6
作者：
Muraki K;Ohnishi K;Takezawa A;Suzuki H;Hatano N;Muraki Y;Hamzah N;Foster R;Waldmann H;Nussbaumer P;Christmann M;Bon RS;Beech DJ
通讯作者：
Beech DJ