酪胺对小鼠三叉神经节神经元A型钾通道的影响

EFFECTS OF TYRAMINE ON A-TYPE POTASSIUM CURRENTS IN TRIGEMINAL GANGLION NEURONS IN MICE

目的:探讨酪胺对小鼠三叉神经节神经元细胞膜电压依赖性钾通道电流及其兴奋性的影响。方法:急性分离小鼠三叉神经节神经元,采用全细胞膜片钳技术测定不同浓度酪胺(1μM、0.1μM、0.01μM、0.001μM、0.0001μM)对瞬时外向型钾通道(A型钾电流,IA)以及延迟整流型钾通道(IDR)电流的影响,并观察0.1μM的酪胺对电压依赖性钠通道及钙通道的影响。结果:如下浓度的酪胺1μM、0.1μM、0.01μM、0.001μM、0.0001μM对A型钾电流的抑制率分别为(48.21±11.72)%(32.25±2.07)%,(23.84±2.69)%,(16.26±2.72)%及(7.07±2.91)%;0.1μM酪胺对电压依赖性钠通道和延迟整流型钾电流无明显影响,仅对钙电流有轻度的抑制作用,抑制率为(11.34±4.97)%;0.1μM酪胺能增强小鼠三叉神经节神经元的放电频率。结论:酪胺呈浓度依赖性抑制A型钾电流;酪胺通过下调A型钾电流增强三叉神经节神经元的兴奋性,增加TGN(trigeminal ganglion neurons)的伤害性传导,从而降低痛阈,导致疼痛。

Objective： To investigate the effect of tyramine on the voltage dependent potassium currents in trigeminal ganglion neurons in mice. Methods： The trigeminal ganglia neurons in mouse were isolated by collagenase. The effects of different concentration of tyramine （lμM, 0. μM, 0.01μM, 0.001 μM and 0.0001 μM） on the transient outward potassium current （type A potassium current, IA） and delayed rectifier potassium current （IDR） were determined by whole cell patch clamp technique. The effects of 0.1 μM tyramine on voltage-dependent sodium channels, calcium channels and the discharge frequency of trigeminal ganglia neurons were also investigated. Results： Type A potassium current was dose-dependently inhibited by tyramine from lllM to 0.00011μM, and the inhibition rate was （48.21 ± 11.72）%, （32.25±2.07）%, （23.84±2.69）%, （16.26±2.72）% and （7.07±2.91）%, respectively. After elution of tyramine, the amplitude of type A potassium current partially recovered to the pretreatment, whereas the sustained delayed rectifier potassium channel and sodium channel were not significantly affected by 0.1 μM tyramine. In the meantime, 0.1 μM tyramine had a minor inhibition on the calcium channel （11.3±4.97）%. 0.1 pM tyramine could also increase the discharge frequency of trigeminal ganglia neurons. Conclusion： Tyramine inhibited type A potassium current in a concentration-dependent manner. Tyramine enhanced excitability oftrigeminal ganglia neurons through down-regulation of type A potassium current.