BDNF-TrkB signaling pathway is involved in pentylenetetrazoleevoked progression of epileptiform activity in hippocampal neurons in anesthetized rats
BDNF-TrkB signaling pathway is involved in pentylenetetrazoleevoked progression of epileptiform activity in hippocampal neurons in anesthetized rats
复制标题
BDNF-TrkB信号通路参与戊四唑诱发麻醉大鼠海马神经元癫痫样活动的进展
DOI：
10.1007/s12264-013-1326-y
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发表时间：
2013-10-01
影响因子：
5.6
通讯作者：
Wang, Xin
中科院分区：
文献类型：
--
作者：
Liu, Xu;Liu, Jia;Wang, Xin
Pentylenetetrazole (PTZ) is a widely-used convulsant used in studies of epilepsy; its subcutaneous injection generates an animal model with stable seizures. Here, we compared the ability of PTZviathe intravenous and subcutaneous routes to evoke progressive epileptiform activity in the hippocampal CA1 neurons of anesthetized rats. The involvement of the BDNF-TrkB pathway was then investigated. When PTZ was given intravenously, it induced epileptiform bursting activity at a short latency in a dose-dependent manner. However, when PTZ was given subcutaneously, it induced a slowly-developing pattern of epileptogenesis; first, generating multiple population-spike peaks, then spontaneous interictal discharge-like spike, leading to the final ictal discharge-like, highly synchronized bursting fi ring in the CA1 pyramidal layer of the hippocampus. K252a, a TrkB receptor antagonist, when given by intracerebroventricular injection, signifi cantly reduced the probability of multiple population spike peaks induced by subcutaneous injection of PTZ, delayed the latency of spontaneous spikes, and reduced the burst frequency. Our results indicate that PTZ induces a progressive change of neuronal epileptiform activity in the hippocampus, and the BDNF-TrkB signaling pathway is mainly involved in the early phases of epileptogenesis, but not the synchronized neuronal burst activity associated with epileptic seizure in the PTZ animal model. These results provide basic insights into the changing pattern of hippocampal neuronal activity during the development of the PTZ seizure model, and establish anin vivoseizure model useful for future electrophysiological studies of epilepsy.
