TrkB,P75～(NTR) Expression In Hippocampus Of Rat Model Of Temporal Lobe Epilepsy And Effected By Topiramate

Objective To characterize the acute and chronic behavioral and histological changes of a temporal lobe epilepsy(TLE) rat model induced by kainic acid(KA) and with therapy of topiramate; and study the brain derived neurotrophic factor(BDNF) receptor TrkB and P75NTR expression in hippocampus;then explore the effect of TrkB and P75NTR in TLE and the antiepileptic mechanism of topiramate. Methods Adult rats were made to be a model of TLE by intraventriculation of KA inducing status epilepticus.The animals were divided into three groups (1) KA group:kindling rats,without therapy of topiramate;(2) KA + TPM group:kindling rats,with therapy of topiramate;(3)N group:normal group;Then divided each groups of kindling rats into five groups at the time point of 1d ,1w,2w,3w,4w .Behavioural evidence was observed; TrkB and P75NTR protein was studied by immunohistochemistry ;hippocampal neuron loss was detected by Nissl's staining. Results (1)Observation of the praxiology:77.1 percent of the rats in KA group appeared status epilepsy and all rats appeared chronic spontaneous seizures. 23.3 percent of the rats in KA+TPM group appeared status epilepsy.only some of them appeared chronic spontaneous seizures and the death date was lower than that in the KA group .No seizure was observed in N group.(2)Cellular morphologic change:In KA groups,within the two weeks after KA-induced SE,cell loss in CA1 pyramidal cells and hillar neurons was prominent but limited;After two weeks of KA-induced SE,cell loss in these regions was markedly enhancing and defusing to CA3 pyramidal cells,achieving peak in the forth week of KA-induced SE.In KA+TPM...