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目的:检测大鼠满性心肌梗死所致心绞痛之后,内侧前额叶皮质(medial prefrontal cortex,mPFC)锥体细胞突触传递活性的变化,探讨调节慢性心绞痛可能的中枢机制。方法:雄性成年SD大鼠随机分为假手术组和慢性心肌梗死(chronic myocardial infarction,CMI)手术组,每组5只。手术2周后,制备mPFC区域急性脑片,通过全细胞膜片钳方法记录锥体细胞的兴奋性和抑制性突触电流,比较假手术组和手术组的突触电流活性变化。结果:相较于假手术组动物,手术组动物mPFC内兴奋性突触电流传递明显增强,抑制性突触电流传递明显减弱。同时抑制性中间神经元动作电位释放下降。结论:CMI之后mPFC内锥体细胞的兴奋性突触信号传递增强,可能是由于局部抑制性神经元活性降低所致。鉴于mPFC内锥体细胞活性对于镇痛具有正向效应,这种变化对于mPFC对慢性心绞痛的中枢抑制可能具有积极的意义。
OBJECTIVE: To detect the changes of synaptic transmission of medial prefrontal cortex (mPFC) pyramidal cells in rats with myocardial infarction-induced angina pectoris and to explore the possible central mechanism of regulating angina pectoris. Methods: Male adult SD rats were randomly divided into sham operation group and chronic myocardial infarction (CMI) operation group, with 5 rats in each group. After 2 weeks of operation, acute cerebral slices of mPFC area were prepared. The excitability and inhibitory synaptic currents of pyramidal cells were recorded by whole-cell patch-clamp method. The changes of synaptic current were compared between the sham operation group and the operation group. Results: Compared with the sham group, the excitatory synaptic currents in the mPFCs increased significantly and the inhibitory synaptic currents decreased significantly. At the same time inhibit the action potential of interneurons decreased. CONCLUSIONS: The excitatory synaptic signal transmission in pyramidal neurons of mPFC after CMI enhancement may be due to the decrease of local inhibitory neuronal activity. Given the positive effect of pyramidal cell activity within mPFC on analgesia, this change may have a positive effect on the central inhibition of mPFC on chronic angina.