目的探讨化学刺激硬脑膜传人神经末梢对大鼠三叉神经节神经元的高电压激活钙电流(HVA.Ica)的调控效应。方法雄性SD大鼠16只按随机数字表法分为生理盐水(NS)组和致炎剂fIS)+释放降钙素基因相关肽(CGRP)组(n=8),大鼠上矢状窦处脑膜给药造模1h后急性分离大鼠三叉神经节中小神经元.采用全细胞膜片钳技术记录电压门控钙离子通道(VGCC)电流。结果与NS组钙电流峰电流[(-49.5±5.18)pA/pF]比较,IS+CGRP组[(-80.48±4.43)pA/pF]增高,差异有统计学意义(P〈0.05);IS+CGRP组神经元钙电流激活曲线的半数激活电压Va1/2为(-20.9±0.4)mV.较NS组[(-16.2±0.5)mV]向超级化方向移动了4.7mV,差异有统计学意义(P〈0.05);IS+CGRP组神经元钙电流的半数失活电压vi1/2为(-12.4±0.2)mV,较NS组[(-22.5±0.3)mV]向去极化方向移动了10.1mV,差异有统计学意义(P〈0.05)。结论激活硬脑膜传人神经末梢诱导初级感觉神经元的外周敏化过程,突出表现为钙电流的增高。
Objective To investigate the modulation of sensitization of dural afferent nerve endings on high voltage active calcium currents (HVA-Ic) of primary sensory neurons from rat trigeminal ganglion. Methods Male adult SD rats were randomly divided into normal saline treatment group (NS, n=8) and proinflammatory agent plus calcitontin gene-related peptide infusion group (IS+CGRP, n=8). One h after the infusion, the effect of CGRP on currents of voltage-gated calcium channel (VGCC) in neurons acutely isolated from trigeminal ganglion was recorded using a conventional whole-cell recording patch clamp technique. Results The peak level of calcium current in the IS+CGRP group ( [-80.48±4.43] pA/pF) was significantly increased as compared with that in the NS group ([-49.5±5.18] pA/pF); the half-activation voltage (V,1/2) in the activation curve of calcium current in the IS±CGRP group ([-20.9±0.4] mV) moved 4.7 mV to the hyperpolarization direction as compared with that in the NS group ([-16.2±0.5] mV) with significant difference (P〈0.05); the half-inactivation voltage (Vi1/2) in the activation curve of calcium current in the IS+CGRP group ([-12.4±0.2] mV) moved 10.1 mV to the depolarization direction as compared with that in the NS group ([-22.5±0.3] mV) with significant difference (P〈0.05). Conclusion Sensitization of dural afferent nerve endings facilitates peripheral sensitization of primary sensory neurons, with an outstanding performance as increment of calcium currents.