Abstract

Objective To study the correlation of neural cell adhesion molecule 1 (NCAM1) with pathogenesis of cognitive dysfunction in epileptic rats and explore its effect on cognitive dysfunction in epileptic rats.Methods A total of 120 Wistar rats were randomly assigned to control group (n=20) and experimental group (n=100); and rats in the experimental group were subdivided into 5 groups (n=20),the epilepsy models were induced by pilocarpine,and rats in these 5 groups received daily treatments for 30 days with either saline,carbamazine,oxcarbazine,aniracetam or donepezil (nootopic).Spatial learning and memory abilities were assessed with Water Maze test.Hippocampus tissue was assessed for NCAM1 mRNAs by RT-PCR and proteins by immunochemistry.Results The mean escape latency of rats in the Morris water maze test:carbamazepine treatment group >oxcarbazepine treatment group >aniracetam treatment group >epilepsy group >donepezi treatment group; significant differences were noted between each two groups (F=91.920,P=0.000).Immunohistochemical and RT-PCR results:donepezi treatment rgroup >aniracetam treatment group >epileptic group >oxcarbazepine treatment group >carbamazepine treatment group> control group; there were differences between each 2 groups (Immunohistochemical result:F=324.510,P=0.000; RT-PCR result:F=81.160,P=0.000).Conclusion NCAM1 expression in the hippocampus rises within 30 days of epileptic attack,who participates in the pathogenesis of cognitive dysfunction; carbamazepine can aggravate the cognitive dysfunction and donepezil can obviously improve the cognitive function of epilepsy. Key words: Epilepsy; Neural cell adhesion molecule 1; Cognitive dysfunction

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call