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目的:研究引起晕动病发生的双轴旋转运动刺激前庭感受器后,中央杏仁核神经元电学反应的变化,探讨中央杏仁核在晕动病(MS)发病中的作用。方法:10只幼年SD大鼠分成两组:对照组和旋转刺激组。旋转刺激组动物经2 h双轴旋转运动刺激(大、小转盘分别以168°/s和432°/s的角速度旋转)。取脑、切片(300μm),应用脑片膜片钳全细胞记录技术记录中央杏仁核神经元膜的主动反应特性以及自发的兴奋性突触后电流(sE PSCs)变化,统计分析、比较两组间的差异。结果:旋转运动刺激后,中央杏仁核神经元电学特性,如膜电位水平(对照组为(-62.80±2.69)mV,旋转组为(-61.37±1.50)mV)以及动作电位(AP)形态未发生显著变化。AP的幅值、半幅时程、最大上升/下降斜率、刺激阈电位和基强度等在两组间没有显著性差别;旋转刺激后,sE PSCs频率从正常组的(0.88±0.42)Hz增加到旋转组的(1.69±0.30)Hz(P<0.05)而幅值(正常组(20.07±3.01)pA;旋转组(21.03±1.44)pA)未发生变化。结论:引发晕动病的运动刺激可引起中央杏仁核神经元兴奋性突触活动增加,突触前谷氨酸释放增加;中央杏仁核参与晕动病反应。
Aims: To investigate the changes of electrical activity of central amygdaloid nucleus after biaxial rotation induced by motion sickness, and to explore the role of central amygdala in the pathogenesis of motion sickness (MS). Methods: Ten young SD rats were divided into two groups: control group and rotational stimulation group. The animals in rotation group were stimulated by two-axis biaxial rotation (large and small carousels rotated at 168 ° / s and 432 ° / s angular velocity respectively). The brain slices were sliced (300μm), and the active response characteristics of central amygdala neurons membrane and spontaneous excitatory postsynaptic currents (sE PSCs) were recorded by whole-cell patch-clamp technique. Statistical analysis was performed. The difference between. Results: The electrical properties of central amygdala neurons such as membrane potential (-62.80 ± 2.69 mV in control group, (-61.37 ± 1.50) mV in rotation group) and AP Significant changes occurred. There was no significant difference between the two groups in amplitude, half-length time history, maximum rise / fall slope, stimulation threshold potential and basal intensity. The frequency of sE PSCs increased from (0.88 ± 0.42) Hz in normal group to The rotation amplitude (1.69 ± 0.30) Hz (P <0.05) and amplitude (20.07 ± 3.01 pA in the normal group and 21.03 ± 1.44 pA in the rotation group did not change. CONCLUSIONS: The motor stimulation of motion sickness can cause the excitatory synaptic activity of central amygdala neurons to increase and the pre-synaptic glutamate release increase. The central amygdala participates in motion sickness.