Objective: Aquaporin4 is the main water channel in the brain that is associated with neurological disorders. The role and the expressive changes of aquaporin4 in epilepsy are still limited and controversial. The study aims to evaluate the expression of c-fos and aquaporin4 during epileptogenesis after systemic kainic acid-induced status epilepticus in the temporal lobe epilepsy animal model and to investigate their alterations in both hippocampus and amygdala.

Methods:

Intraperitoneal injections of kainic acid (5-15 mg/kg) by repeated low kainic acid protocol were given to young adult 32 Wistar albino rats for status epilepticus. Aquaporin4 and c-fos were investigated in the hippocampus and amygdala on days 1 and 60 after status epilepticus by immunostaining methods in brain slices.

Results:

The intensity of c-fos immunostaining rose considerably in the hippocampus CA1 area of rats during the acute period (P < 0.05) and in the amygdala during the chronic period. The immunostaining intensity of aquaporin4in the hippocampus of rats with acute kainic acid increased significantly (P < .05). It was also raised in the hippocampal region of the rats in the acute sham and chronic kainic acid groups.

Discussion:

The results of this study support a link between aquaporin4 and epilepsy. It can be speculated that aquaporin4 change is primarily a defense mechanism immediately after status epilepticus, and then, it can evolve into a causal factor with exhaustion as a result of overuse.

Keywords: c-fos, AQP4, epileptogenesis, temporal lobe epilepsy, animal model, kainic acid