Interference of TRPV1 function altered the susceptibility of PTZ-induced seizures | |
Jia YF1,2; Li YC1,3; Tang YP1,2; Cao J1,2; Wang LP1,2; Yang YX1,2; Xu L[*]1,2; Mao RR[*]1,2 | |
刊名 | FRONTIERS IN CELLULAR NEUROSCIENCE |
2015 | |
卷号 | 9期号:X页码:e20 |
关键词 | TRPV1 capsaicin capsazepine seizure hippocampus pentylenetetrazol |
通讯作者 | lxu@vip.163.com ; talktomaomao@163.com |
合作状况 | 其它 |
英文摘要 | Transient receptor potential vanilloid 1 (TRPV1) is widely distributed in the central nervous system (CNS) including hippocampus, and regulates the balance of excitation and inhibition in CNS, which imply its important role in epilepsy. We used both pharmacological manipulations and transgenic mice to disturb the function of TRPV1 and then studied the effects of these alterations on the susceptibility of pentylenetetrazol (PTZ)-induced seizures. Our results showed that systemic administration of TRPV1 agonist capsaicin (CAP 40 mg/kg) directly induced tonic-clonic seizures (TCS) without PTZ induction. The severity of seizure was increased in lower doses of CAP groups (5 and 10 mg/kg), although the latency to TCS was delayed. On the other hand, systemic administration of TRPV1 antagonist capsazepine (CPZ, 0.05 and 0.5 mg/kg) and TRPV1 knockout mice exhibited delayed latency to TCS and reduced mortality. Furthermore, hippocampal administration of CPZ (10 and 33 nmol/mu L/side) was firstly reported to increase the latency to TCS, decrease the maximal grade of seizure and mortality. It is worth noting that decreased susceptibility of PTZ-induced seizures was observed in hippocampal TRPV1 overexpression mice and hippocampal CAP administration (33 nmol/mu L/side), which is opposite from results of systemic agonist CAP Our findings suggest that the systemic administration of TRPV1 antagonist may be a novel therapeutic target for epilepsy, and alteration of hippocampal TRPV1 function exerts a critical role in seizure susceptibility. |
收录类别 | SCI |
资助信息 | This work was supported by grants from National Basic Research Program of China (2013CB835103), Strategic Priority Research Program of the Chinese Academy of Science (XDB02020002), the National Natural Science Foundation of China (31100786, 81171294, U1032605, and U1132602), Science and Technology Program of Yunnan Province (2013GA003, 2010CD104, and 2013FA048). |
语种 | 英语 |
WOS记录号 | WOS:000349601400001 |
公开日期 | 2015-03-13 |
内容类型 | 期刊论文 |
源URL | [http://159.226.149.42:8088/handle/152453/8278] |
专题 | 昆明动物研究所_学习记忆的分子神经机制 昆明动物研究所_动物模型与人类重大疾病机理重点实验室 |
作者单位 | 1.Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences & Yunnan Province, and KIZ/CUHK Joint Laboratory of Bioresources and Mol 2.Kunming College of Life Science, University of Chinese Academy of Sciences, Beijing, China 3.School of Life Sciences, University of Science and Technology of China, Hefei, China |
推荐引用方式 GB/T 7714 | Jia YF,Li YC,Tang YP,et al. Interference of TRPV1 function altered the susceptibility of PTZ-induced seizures[J]. FRONTIERS IN CELLULAR NEUROSCIENCE,2015,9(X):e20. |
APA | Jia YF.,Li YC.,Tang YP.,Cao J.,Wang LP.,...&Mao RR[*].(2015).Interference of TRPV1 function altered the susceptibility of PTZ-induced seizures.FRONTIERS IN CELLULAR NEUROSCIENCE,9(X),e20. |
MLA | Jia YF,et al."Interference of TRPV1 function altered the susceptibility of PTZ-induced seizures".FRONTIERS IN CELLULAR NEUROSCIENCE 9.X(2015):e20. |
个性服务 |
查看访问统计 |
相关权益政策 |
暂无数据 |
收藏/分享 |
除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。
修改评论