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背景:纳洛酮的促醒机制不可能完全是因为抑制内源性阿片肽所致,所以进一步探讨纳洛酮逆转昏迷作用的神经药理机制,具有重要意义。目的:观察促醒剂纳洛酮对大鼠额叶皮质神经元兴奋性的影响,以了解纳洛酮是否通过非阿片受体抑制机制发挥促醒作用。设计:两因素析因设计。单位:解放军第一六一中心医院神经内科;华中科技大学同济医学院同济医院神经内科。材料:实验于2003-12/2004-04在华中科技大学同济医学院实验中心完成。选取出生8～12d健康Wistar大鼠30只,体质量150～250g,雌雄不限。方法:实验在20～24℃的室温下进行。选择表面光洁,胞体呈三角形或锥形且折光性强,有一个以上突起的神经元进行膜片钳实验。实验给药方法包括灌流给药(γ氨基丁酸)和压力喷射给药(谷氨酸和纳洛酮等)。主要观察指标:谷氨酸和γ氨基丁酸及纳洛酮对急性分离的FCX锥体细胞兴奋性的影响。结果:急性分离的皮质神经元能对兴奋性性神经递质谷氨酸和抑制性神经递质γ氨基丁酸产生正常反应。电流钳记录模式下,纳洛酮(0.1mmol/L)使额叶皮质神经元去极化伴动作电位发放频率增加,电压钳记录模式下,纳洛酮(0.1mmol/L)使神经元产生内向电流(13/14)。结论:纳洛酮对皮质神经元具有直接兴奋作用,提示其可通过直接兴奋皮质,发挥逆转昏迷,促觉醒作
BACKGROUND: The mechanism of naloxone’s arousal can not be completely attributed to the inhibition of endogenous opioid peptides. Therefore, it is of great significance to further explore the neuropharmacological mechanism of naloxone in reversing the effects of coma. OBJECTIVE: To observe the effect of naloxone on the excitability of frontal cortex neurons in rats in order to find out whether naloxone exerts an arousal effect through the non-opioid receptor inhibitory mechanism. Design: Two factorial factorial design. Unit: Department of Neurology, No.161 Central Hospital of PLA; Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology. MATERIALS: Experiments were performed at the Experimental Center, Tongji Medical College, Huazhong University of Science and Technology from December 2003 to April 2004. Thirty healthy Wistar rats aged 8-12 days were selected and their body weight was 150-250 g. Methods: The experiment was carried out at room temperature of 20 ~ 24 ℃. Select the surface smooth, cell body was triangular or conical and refractive strong, more than one neuron protruding patch clamp experiments. Experimental methods of administration include perfusion (gamma aminobutyric acid) and pressure jet administration (glutamic acid and naloxone, etc.). MAIN OUTCOME MEASURES: Effects of glutamate, γ-aminobutyric acid and naloxone on the excitability of acutely isolated FCX pyramidal cells. RESULTS: Acutely isolated cortical neurons produced a normal response to the excitatory neurotransmitter glutamate and the inhibitory neurotransmitter γ-aminobutyric acid. In current clamp recording mode, naloxone (0.1 mmol / L) increased the depolarization frequency of the frontal cortex neurons and the release of action potential. Naloxone (0.1 mmol / L) produced neurons in voltage clamp recording mode Inward current (13/14). Conclusion: Naloxone has a direct excitatory effect on cortical neurons, suggesting that it may directly activate the cortex, exert a reversal of coma and awakening