Effects of melatonin on expression of GluR2 in the hippocampus and cognitive function of rat models of epilepsy
10.3969/j.issn.2095-4344.2015.27.012
- VernacularTitle:抑黑素对癫痫模型大鼠海马区GluR2表达及认知功能的影响
- Author:
Yan XU
;
Ziliang TIAN
;
Bin PANG
- Publication Type:Journal Article
- Keywords:
Tissue Engineering;
Epilepsy;
Cognition;
Hippocampus
- From:
Chinese Journal of Tissue Engineering Research
2015;(27):4328-4332
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:Current research data have shown that patients with epilepsy are often accompanied by complications such as cognitive impairment. Recent studies have demonstrated that melatonin has an inhibitory effect on epilepsy, but its underlying mechanism is unknown. OBJECTIVE: To investigate the effects of melatonin on the cognitive function and GluR2 expression in the hippocampus of rat models of epilepsy, and further study the mechanism of melatonin against epilepsy. METHODS: Rat models of chronic epilepsy were established by intraperitoneal injection of lithium chloride-pilocarpine, and intraperitonealy injected with sufficient amount of physiological saline and melatonin respectively. Control group was set for observation. RESULTS AND CONCLUSION:At 4 and 6 weeks after modeling, the GluR2 expression level in the hippocampus of rats in the epilepsy + melatonin group was significantly higher than that in the epilepsy group (P < 0.05); the GluR2 expression level in the synaptic membrane of hippocampal CA1 region of rats in the control and epilepsy + melatonin groups was significantly higher than that in the epilepsy group (P < 0.05). At 4 days after modeling, compared with epilepsy group and epilepsy + physiological saline group, the escape latency, operation time, active avoidance latency, passive avoidance latency of rats in the epilepsy + melatonin group were significantly decreased (P< 0.05), the correct rate and active avoidance number were significantly increased (P < 0.05). These results demonstrate that melatonin can improve the cognitive function of rat models of epilepsy by up-regulating the expression of GluR2 in the synaptic membrane of hippocampal CA1 region.
