Background and Aim: In epileptic patients, behavioral disorders are the most important deficits therefore evaluation of deficits by animal model should be essential. The role of Zinc in behavioral disorder and its relation with hippocampus or serum zinc may help explain why some brain region is commonly facilitated while other did not harm. The main purpose of this study was to evaluate Zinc itself effect on changing behavioral disorder and control of brain seizure.
Materials and Methods: Type of this study is prospective, empirical and blind. The population was adult male Sprauge-Dawley rats and randomly assigned in six groups (n=8). Each group was treated two months before of inducing animal model of seizure by Zinc(248 mg/lit) or tap water and also in group 1 and 4 saline, group 2and 5 bicuculine(1mg/kg) and group 3 and 6 pentobarbital(10mg/kg) .epileptic model was induced by injection of Lithium chloride (127mg/kg)and 24 hr later ,pilocarpin(50 mg/kg) in to peritoneum. During this study, neurological deficits (behavior) was recorded at 1, and 2 hrs after sizuring.
Results: The results showed that Zn had a minus feature on neurological deficits. GABA A antagonists had the same effect as Zn on neurological deficits but GABA A agonists ameliorate it significantly. Serum zinc level didn&apost change significantly among the animals but hippocampus zinc was altered significantly in Zn treated animals compared with the controls.
Conclusion: This study shows that Zn deleterious effects on neurological deficits were carried out via GABAergic system.
