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[The relations between electrical synapse and the mechanism of epilepsy in genetical epilepsy-prone rat]
1Department of Child Neurology, First Teaching Hospital, Beijing Medical University.
Objective:
To investigate the role of gap junction protein Cx32 formed electrical synapses in the pathogenesis of epilepsy.
Methods:
Antisense oligodeoxynucleotides (ODN) techniques, intracerebroventricular injection, neuronal discharges in temporal cortex slices, in situ hybridization and immunohistochemistry were used.
Results:
An antisense ODN for Cx32 100 micrograms was intracerebroventricularly injected once daily, for 3 days to P77PMC rat. The audiogenic seizure scores were significantly lowered as compared with the corresponding sense ODN (or PBS) treated control groups. Moreover, in the enterhinal cortex of the temporal cortex slice of antisense ODN treated P77PMC rat, the typical seizure like events and the late recurrent discharges were not induced by lower Mg2+ solution. The frequency and amplitude of neuronal discharges were decreased as compared with the control group. In situ hybridization and immunohistochemistry studies confirmed that Cx32 mRNA expression and Cx32 synthesis were also inhibited by Cx32 antisense ODN in P77PMC rat brain.
Conclusion:
Our results confirmed that gap junction formed electrical synapse between neurons plays an important role in the development of synchronization of neuronal discharges in vivo and in vitro.