摘要
运用细胞内记录和全细胞膜片钳技术 ,在 7～ 16d大鼠带三叉神经残根的 4 0 0 μm厚脑桥切片上进行研究。细胞内电流钳记录显示三叉神经主核灌流甘丙肽引发两种膜电位变化 :54.2 %细胞超极化 (3.2±1.2 )mV ;35.4 %细胞去极化 (2 .9± 1.3)mV ,两者均伴有兴奋性突触后电位抑制和膜电阻减小。电压钳实验显示甘丙肽也引致两种膜电流变化 :57.9%细胞出现外向性电流 (11.6± 6 .1)pA ,该电流可被四乙基胺所抑制 ,其反转电位为 (- 77.1± 5.3)mV ;2 7.3%细胞出现内向性电流 (10 .9± 5.9)pA ,该电流可被细胞外低钠所抑制而被细胞外高钾所增强 ,其反转电位为 (- 2 9.2± 4 .3)mV。两电流均可被甘丙肽激动剂M16所模拟 ,为甘丙肽阻断剂M35和M4 0所阻抑。上述结果提示 ,甘丙肽在突触后膜引发两种不同的膜电活动 :钾离子外流引发超极化和外向性电流 ;钠离子内流和钾离子外流引发去极化和内向性电流 ,两种反应均能抑制三叉神经主核神经元的突触传递。
To determine the effect of galanin (Gal) and its ion machanism involved onmembrane electric activities of principal trigeminal nucleus (PrV) neurons of neonatal rats in vitro, studies were carried out on 400 μm thick pontine slices of this nucleus and the trigeminal root in rats aged 7-16 days by using intracellular recording and whole-cell patch clamp techniques. Excitatory postsynaptic potentials (EPSPs) were evoked by electrical stimulation of the trigeminal root. In current-clamp mode administration of 0.3 μmol/L Gal to PrV elicited two types of membrane potentials: hyperpolarization by (3.2±1.2)mV in 54.2% cells (26/48) tested and depolarization by (2.9±1.3)mV in 35.4% cells (17/48), each response was associated with a decrease in EPSPs and membrane resistance. In voltage-clamp mode 0.3 μmol/L Gal perfused to PrV evoked a couple of membrane currents: an outward current of (11.6± 6.1) pA (57.9%; 51/88) and an inward current of (10.9±5.9) pA (27.3%; 24/88). The former had a mean reversal potential of (-77.1±5.3)mV and was reversibly abolished by tetraethylammonium (TEA), and the latter had a mean reversal potential of (-29.2±4.3)mV and reduced in a Na+-free medium or increased in a high K+ medium. Both currents were mimicked by Gal agonist M16 and antagonized by Gal antagonist M35 or M40. These results suggest that Gal postsynaptically elicits a couple of distinct membrane electric activities: (A) a K+-outward movement induces hyperpolarization and an outward current, (B) a mixed movement of K+-outward and Na+-inward induces depolarization and an inward current. Both responses attenuate PrV neuron synaptic transmission.
