OBJECTIVE: To investigate the expression of neural growth-associated protein (GAP-43) and synaptophysin (P38) gene and protein in insular electrical kindled epileptic rats and its significance. METHODS: Seventy-two male adult rats were divided into kindled group (n = 36) and sham group (n = 36) randomly. Each group was further divided into 1, 3, 7, 15, 30 and 60 d sub-groups (n = 6) respectively. After kindling with immunohistochemical staining and hybridization in situ, the altered expressions of GAP-43 and P38 were detected in hippocampus of insular electrical kindled epilepsy rats. RESULTS: Epilepsy day 1: GAP-43 mRNA and protein expression at hippocampus dentate gyrus granular cell layer, hilus and CA3 pyramidal layer in the kindled group were higher than the sham group (P < 0.05). The expressions declined at Day 3 (P > 0.05). Expressions became elevated again at Day 7 and they were significantly higher than those in the sham group at Days 15 and 30 (P < 0.05). There was no statistical difference between two groups at Day 60 (P > 0.05). Expressions of P38 mRNA and protein: hybridization signal and immunostaining at hippocampus dentate gyrus granular cell layer, hilus and CA3 pyramidal layer began to rise at Day 7 and peaked at Day 15 (P < 0.01). They lasted 4 weeks and then began to decline. CONCLUSION: Insular epilepsy is closely related with temporal hippocampus. GAP-43 and P38 may be the pathological basis of insular epilepsy and the key molecular mechanism of synaptic plasticity.
OBJECTIVE: To investigate the expression of neural growth-associated protein (GAP-43) and synaptophysin (P38) gene and protein in insular electrical kindled epilepticrats and its significance. METHODS: Seventy-two male adult rats were divided into kindled group (n = 36) and sham group (n = 36) randomly. Each group was further divided into 1, 3, 7, 15, 30 and 60 d sub-groups (n = 6) respectively. After kindling with immunohistochemical staining and hybridization in situ, the altered expressions of GAP-43 and P38 were detected in hippocampus of insular electrical kindled epilepsyrats. RESULTS:Epilepsy day 1: GAP-43 mRNA and protein expression at hippocampus dentate gyrus granular cell layer, hilus and CA3 pyramidal layer in the kindled group were higher than the sham group (P < 0.05). The expressions declined at Day 3 (P > 0.05). Expressions became elevated again at Day 7 and they were significantly higher than those in the sham group at Days 15 and 30 (P < 0.05). There was no statistical difference between two groups at Day 60 (P > 0.05). Expressions of P38 mRNA and protein: hybridization signal and immunostaining at hippocampus dentate gyrus granular cell layer, hilus and CA3 pyramidal layer began to rise at Day 7 and peaked at Day 15 (P < 0.01). They lasted 4 weeks and then began to decline. CONCLUSION:Insular epilepsy is closely related with temporal hippocampus. GAP-43 and P38 may be the pathological basis of insular epilepsy and the key molecular mechanism of synaptic plasticity.