大鼠杏仁核电刺激癫痫持续状态后颞叶癫痫模型海马区神经生长相关蛋白43的表达

Expression of GAP-43 in hippocampus of rat model of temporal lobe epilepsy after status epilepticus induced by electrical stimulation of amygdala

摘要:

目的 探讨神经生长相关蛋白43（GAP-43）在大鼠杏仁核电刺激癫痫持续状态后颞叶癫痫（SE）模型海马区的表达及意义。方法 健康雄性Wistar大鼠60只，分成4组：空白对照组、未刺激组、未发作组和发作组。空白对照组：不植入电极；未刺激组：植入电极未行电刺激；发作组：植入电极电刺激后15 d内、30 d内能观察到稳定的自发性反复发作（SRS）的大鼠归为发作组，其余归为未发作组。分别在15 d、30 d时，将标本应用RT-PCR及免疫荧光检测方法检测大鼠海马GAP-43的表达。结果 致痫15 d，发作组、未发作组和未刺激组的GAP-43表达高于空白对照组，并依次降低（P<0.05）。致痫30 d，发作组和未发作组GAP-43表达仍高于空白对照组，差异有统计学意义（P<0.05）；未刺激组与空白对照组水平相当，二者差异无统计学意义（P>0.05）。结论 GAP-43参与了神经元损伤修复和突触重塑，其可能是颞叶癫痫的病理基础——突触重塑的重要分子机制。

Abstract:

Objective To investigate the expression of growth-associated protein-43 (GAP-43) in the hippocampus of rat model of temporal lobe epilepsy (TLE) after status epilepticus induced by electrical stimulation of the amygdala and its significance.Methods Sixty healthy male Wistar rats were divided into blank control, unstimulated, non-seizure, and seizure groups. The blank control group had no implanted electrodes;the unstimulated group had implanted electrodes, but did not undergo electrical stimulation;the seizure group had spontaneous recurrent seizure within 15 and 30 days after electrical stimulation through implanted electrodes;other rats were included in the non-seizure group. The expression of GAP-43 in the hippocampus of rats was evaluated by RT-PCR and immunofluorescence assay at 15 and 30 days after electrical stimulation.Results At 15 days after electrical stimulation, the seizure, non-seizure, and unstimulated groups had significantly higher expression of GAP-43 than the blank control group, and GAP-43 expression decreased significantly from the seizure group to the blank control group (P<0.05). At 30 days after electrical stimulation, the seizure and non-seizure groups still had significantly higher expression of GAP-43 than the blank control group (P<0.05);there was no significant difference in GAP-43 expression between the unstimulated and blank control groups (P>0.05).Conclusions GAP-43 is involved in the damage repair and synaptic plasticity of neurons, which may be the pathological basis of TLE and the important molecular mechanism of synaptic plasticity.