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STK24 modulates excitatory synaptic transmission in epileptic hippocampal neurons.

Authors
  • Yang, Juan1
  • Jiang, Qian1
  • Yu, Xinyuan1
  • Xu, Tao1
  • Wang, You1
  • Deng, Jing1
  • Liu, Yong1
  • Chen, Yangmei1
  • 1 Department of Neurology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, China. , (China)
Type
Published Article
Journal
CNS Neuroscience & Therapeutics
Publisher
Wiley (Blackwell Publishing)
Publication Date
Aug 01, 2020
Volume
26
Issue
8
Pages
851–861
Identifiers
DOI: 10.1111/cns.13391
PMID: 32436359
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

A large amount of literature has indicated that excitatory synaptic transmission plays a crucial role in epilepsy, but the detailed pathogenesis still needs to be clarified. In the present study, we used samples from patients with temporal lobe epilepsy, pentylenetetrazole-kindled mice, and Mg2+ -free-induced epileptic cultured hippocampal neurons to detect the expression pattern of STK24. Then, the whole-cell recording was carried out after STK24 overexpression in the Mg2+ -free-induced epileptic cultured hippocampal neurons. In addition, coimmunoprecipitation was performed to detect the association between endogenous STK24 and main subunits of NMDARs and AMPARs in the hippocampus of PTZ-kindled mice. Here, we reported that STK24 was specifically located in epileptic neurons of human and pentylenetetrazole-kindled mice. Meanwhile, the expression of STK24 was significantly down-regulated in these samples which are mentioned above. Besides, we found that the amplitude of miniature excitatory postsynaptic currents was increased in STK24 overexpressed epileptic hippocampal cultured neurons, which means the excitatory synaptic transmission was changed. Moreover, the coimmunoprecipitation, which further supported the previous experiment, indicated an association between STK24 and the subunits of the NMDA receptor. These findings expand our understanding of how STK24 involved in the excitatory synaptic transmission in epilepsy and lay a foundation for exploring the possibility of STK24 as a drug target. © 2020 The Authors. CNS Neuroscience & Therapeutics Published by John Wiley & Sons Ltd.

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