目的：观察低温在治疗癫痫发生过程中的细胞学机制。方法使用单-双-膜片钳技术，对4-氨基吡啶诱导的癫痫小鼠模型的海马和皮层神经元细胞进行穿孔，分别记录不同温度下细胞的电生理变化。结果持续低温能阻断4-氨基吡啶诱导的海马神经元的持续性放电并增加输入电阻。通过双-膜片钳记录显示相距较远的 CA1和 CA3区域的锥体神经元有显著的同步性，但锥体神经元和中间神经元间的同步性较弱。在CA1和CA3神经元中，低温可以阻断节律性动作电位的放电行为，并能破坏其同步性；但在中间神经元中低温阻断节律性放电时并不会破坏动作电位。结论低温对γ-氨基丁酸传导和分泌影响程度不同，干扰了神经网络的同步放电，从而阻断癫痫样放电。另外，γ-氨基丁酸释放导致的中间神经元动作电位持续放电，也增强了低温的抗癫痫作用。%Objective To investigate the cytological mechanism of the low temperature for treating the epilepsy occurrence process.Methods The hippocampus and cortex neurons in the 4-aminopyridine induced mouse epilepsy model were performed the perforation by using the single-and dual-patch clamp technique and the electrophysiologic changes under different temperatures were recorded respectively.Results The continuous low temperature could block the continuous discharge of the hippocampus neurons induced by 4-aminopyridine and increase the input resistance.The dual-patch clamp recordings showed that the pyramidal neurons in the CA1 and CA3 regions far apart from each other had the significant synchronism,but the synchronism between the pyramidal neurons and interneurons was weaker.In CA1 and CA3 neurons,hypothermia could block the rhythmic action potential discharges and destroyed their synchronism;however,in blocking rhythmic discharges of interneurons,hypothermia did not destroy the action potentials.Conclusion Hypothermia affects theγ-aminobutyric acid conduction and secretion to different degrees and interferes the synchronic discharge of neural network,thus blocks the epileptiform discharge.In addition,continuous discharge of interneurons ac-tion potentials induced byγ-aminobutyric acid release would enhance the antiepileptic effects of hypothermia.
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