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目的:观察异丙酚对急性分离的大鼠脊髓背角神经元TTX敏感型钠通道电流的影响及相关机制。方法:取出生后7d的雄性SD大鼠,击昏后断头取脊髓腰膨大部位,分离背角神经元,应用全细胞膜片钳记录模式记录钠电流。距离神经细胞100μm施加0.3~30μmol/L不同浓度的异丙酚,应用-10mV(持续30 ms)刺激电压诱发钠电流,求出异丙酚对钠电流的半效抑制浓度(IC50)。观察异丙酚对钠通道失活效应的影响时,应用从-80mV至-20mV的预刺激电压(阶差为10mV,持续30ms),再应用0mV刺激电压(持续30ms)诱发钠电流产生,向神经细胞施加IC50水平的异丙酚。观察异丙酚对钠通道去失活效应的影响时,应用-10mV的预刺激电压(持续30ms),再给予-10mV、持续30 ms的刺激电压诱发钠电流产生,两刺激电压的间隔时间为2~24ms。结果:异丙酚可浓度依赖性地抑制TTX敏感型钠电流,其IC50为(5.35±0.25)μmol/L。钠通道失活实验中,预刺激电压在-60mV到-40mV范围内,IC50水平的异丙酚可显著抑制由刺激电压(0mV)诱发的钠电流(P<0.05)。钠通道去失活实验中,两刺激的间隔时间在2~6ms之间时,IC50水平的异丙酚可显著性抑制由刺激电压(-10mV)诱发的钠电流(P<0.01,P<0.05)。结论:异丙酚可抑制大鼠脊髓背角电压依赖性钠通道电流,这一作用与促进钠通道的失活和抑制钠通道的去失活有关。
Objective: To investigate the effects of propofol on acutely isolated TTX-sensitive sodium channel currents in rat spinal dorsal horn neurons and its related mechanisms. Methods: Male Sprague-Dawley rats 7 days after birth were taken out of the spinal cord and the dorsal horn was removed after decapitation. The dorsal horn neurons were isolated and the whole-cell patch-clamp recording mode was used to record the sodium current. Propofol of 0.3 ~ 30μmol / L at a concentration of 0.3 ~ 30μmol / L was applied at a distance of 100μm from the nerve cells. The voltage-induced sodium current was applied at -10mV for 30ms, and the half inhibitory concentration (IC50) of propofol on sodium current was calculated. To observe the effect of propofol on inactivation of sodium channels, sodium currents were induced by applying a pre-stimulation voltage of -80 mV to -20 mV (with a step difference of 10 mV for 30 ms) followed by a stimulation voltage of 0 mV (for 30 ms) Neuronal cells were administered propofol at IC50 levels. To observe the effect of propofol on the deactivation of sodium channels, a pre-stimulation voltage of -10 mV (for 30 ms) was applied, and then a -10 mV stimulation voltage was applied for 30 ms to induce sodium current. The interval between two stimulation voltages was 2 ~ 24ms. RESULTS: Propofol inhibited TTX-sensitive sodium currents in a concentration-dependent manner with IC50 of (5.35 ± 0.25) μmol / L. In the inactivation of sodium channels, the pre-stimulation voltage ranged from -60mV to -40mV, and the IC50-level propofol significantly inhibited the sodium current induced by stimulation voltage (0mV) (P <0.05). Sodium channel deactivation experiments showed that propofol at IC50 level significantly inhibited sodium currents induced by stimulation voltage (-10mV) (P <0.01, P <0.05) when the interval between two stimuli was between 2 and 6 ms ). CONCLUSION: Propofol can inhibit the voltage-dependent sodium channel current in the dorsal horn of spinal cord in rats. This effect is related to the inactivation of sodium channels and the deactivation of sodium channels.