Abstract
IntroductionA 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.MethodsIn 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.ResultsHere, 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.ConclusionThese 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.
Highlights
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
The results show that the frequency of action potential (AP) in the Mg2+-free group was significantly higher when compared with the control group (Figure 3A and B) (**P < .01), and this confirms that the model was successfully established
Regulating excitatory synaptic transmission is the key step to control the development of epilepsy.[23,24,25]
Summary
Epilepsy is a chronic brain disease with the repeated, abnormal, and high-synchronization discharge of neurons. The imbalance of excitation and inhibition of the neural circuit is considered to be one of the most important pathogenesis of epilepsy.[4] Dendritic spines, which have mainly involved in the afferent of excitatory signals, are critical for the formation of functional neural circuits.[5]. Serine/threonine kinase 24 (STK24), which belongs to the sterile 20 kinase family, known as mammalian sterile 20-like kinase 3 (MST3), is widely expressed in many tissues including the brain.[6,7] STK24 was reported to facilitate dendritic spine development and maintain the structure of excitatory synapse.[8] Further, STK24 was involved in changing the spontaneous excitatory postsynaptic currents of the mouse cortical pyramidal neurons in upper layers IIIII, which indicates its possible role in regulating cortical excitability.[9] it has not been studied whether STK24 modulates the excitatory synaptic transmission in epilepsy. We determined the possible interaction between STK24 and several main glutamate receptors in the pentylenetetrazole (PTZ)-kindled mouse model
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