| Objective:To study the expression of connexin 43,32 in the hippocampal tissue of epilepsy-rats induced by kainic acid(KA) and the effects of octanol on them,and investigate the role of connexin 43,32 in epileptogenesis and the antiepileptic mechanism of octanol.Methods:SD rats were randomly divided into control group,Kainic acid (KA) group,octanol group and DMSO group,respectively.With stereotaxic apparatus,KA was injected into the rats' amygdaloid nucleus with a density of 1μg/μL for making epileptic models.Rats in KA group,octanol group and DMSO group were divided into five subgroups after KA were injected for 3h,6h,12h,24h and7d,respectively.30 minutes before KA were injected,rats in octanol group were pretreated by intraperitoneal injection of octanol with a density of 5 mmol/kg according to body mass.Octanol was dissolved in DMSO.Rats in DMSO group were intraperitoneally injected with isorrhopic DMSO.Rats in control group were raised without any special treatment.The epilepsy-rats induced by KA and that treated by octanol were assessed by Patel score and their latency of epileptic seizure was recorded.The expression of connexin 43, 32 in the hippocampal tissue was measured by immunohistochemistry.Location of connexin 32 was detected by immunofluorescence.Results:According to HE staining,after KA was injected for 3 hours, slight edema was found in CA2,CA3 regions of the hippocampal tissues of both KA group and octanol group.With the time went on from 3h to 24h,situation of the edema became worsen,but almost disappeared:at 7 days after KA's injection.Compared with KA group,the edema in octanol group manifestly alleviated.The number of neurons in CA2,CA3 regions of the hippompal tissue in KA group and octanol group decreased in the process of KA's treatment,compared with control group.But the decrease in octanol group was lower than that in KA group.The expression Of CX43,CX32 in all regions of the hippocampol tissue in KA group and octanol group gradually increased as the KA's treatment went on,which was differed from that of control group (P＜0.01).Compared with KA group,the expression of both proteins in octanol treated group was lower than that in KA group(P＜0.01).There was no difference between DMSO group and KA group in the expression of CX43 and CX32.The expression of CX32 in immunofluorescence located in plasma and nuclei.It was stronger in both KA group and octanol group than that in control group,butwas lower in octanol group than that in KA group,the Patel score of the rats in octanol group was lower than that in KA group within 3 hours after the induction(P＜0.01),but the latency was longer(P＜0.01).Conclusion:After the epileptic seizure repeatedly,the expression of CX43, CX32 was upregulated,which increased the numbers of gap junction between neuron and glial cell and facilitated synchronous discharge in neurons.So CX43, CX32 were involved in occurrence and development of epilepsy.Treatment of octanol could reduce the expression of connexin 43,32,and alleviate edema in brain,prolong the latency of epileptic seizure and decrease degrees of epileptic seizure.It had manifestly anti-epileptic effect.
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