Open AccessSTK24 modulates excitatory synaptic transmission in epileptic hippocampal neurons
Author(s) -
Yang Juan,
Jiang Qian,
Yu Xinyuan,
Xu Tao,
Wang You,
Deng Jing,
Liu Yong,
Chen Yangmei
Publication year - 2020
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.13391
Subject(s) - excitatory postsynaptic potential , hippocampal formation , neuroscience , neurotransmission , epilepsy , hippocampus , postsynaptic potential , inhibitory postsynaptic potential , chemistry , biology , receptor , biochemistry
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. Methods In the present study, we used samples from patients with temporal lobe epilepsy, pentylenetetrazole‐kindled mice, and Mg 2+ ‐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 Mg 2+ ‐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. Results 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. Conclusion 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.