中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2012年
6期
600-604
,共5页
刘沙%刘欣%武文卉%黄琳%郭永涛%燕兰云%万琪
劉沙%劉訢%武文卉%黃琳%郭永濤%燕蘭雲%萬琪
류사%류흔%무문훼%황림%곽영도%연란운%만기
偏头痛%外周敏化%全细胞记录式膜片钳%钙电流
偏頭痛%外週敏化%全細胞記錄式膜片鉗%鈣電流
편두통%외주민화%전세포기록식막편겸%개전류
Migraine%Peripheral sensitization%Whole cell recording patch clamp%Calcium current
目的 探讨化学刺激硬脑膜传入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(IS)+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Val/2为(-20.9±0.4)mV,较NS组[(-16.2±0.5)mV]向超级化方向移动了4.7 mV,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V1/2为(-12.4±0.2) mV,较NS组[(-22.5±0.3)mY]向去极化方向移动了10.1 mV,差异有统计学意义(P<0.05). 结论 激活硬脑膜传入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.
目的 探討化學刺激硬腦膜傳入神經末梢對大鼠三扠神經節神經元的高電壓激活鈣電流(HVA-ICa)的調控效應. 方法 雄性SD大鼠16隻按隨機數字錶法分為生理鹽水(NS)組和緻炎劑(IS)+釋放降鈣素基因相關肽(CGRP)組(n=8),大鼠上矢狀竇處腦膜給藥造模1h後急性分離大鼠三扠神經節中小神經元,採用全細胞膜片鉗技術記錄電壓門控鈣離子通道(VGCC)電流. 結果 與NS組鈣電流峰電流[(-49.5±5.18)pA/pF]比較,IS+CGRP組[(-80.48±4.43) pA/pF]增高,差異有統計學意義(P<0.05);IS+CGRP組神經元鈣電流激活麯線的半數激活電壓Val/2為(-20.9±0.4)mV,較NS組[(-16.2±0.5)mV]嚮超級化方嚮移動瞭4.7 mV,差異有統計學意義(P<0.05); IS+CGRP組神經元鈣電流的半數失活電壓V1/2為(-12.4±0.2) mV,較NS組[(-22.5±0.3)mY]嚮去極化方嚮移動瞭10.1 mV,差異有統計學意義(P<0.05). 結論 激活硬腦膜傳入神經末梢誘導初級感覺神經元的外週敏化過程,突齣錶現為鈣電流的增高.
목적 탐토화학자격경뇌막전입신경말소대대서삼차신경절신경원적고전압격활개전류(HVA-ICa)적조공효응. 방법 웅성SD대서16지안수궤수자표법분위생리염수(NS)조화치염제(IS)+석방강개소기인상관태(CGRP)조(n=8),대서상시상두처뇌막급약조모1h후급성분리대서삼차신경절중소신경원,채용전세포막편겸기술기록전압문공개리자통도(VGCC)전류. 결과 여NS조개전류봉전류[(-49.5±5.18)pA/pF]비교,IS+CGRP조[(-80.48±4.43) pA/pF]증고,차이유통계학의의(P<0.05);IS+CGRP조신경원개전류격활곡선적반수격활전압Val/2위(-20.9±0.4)mV,교NS조[(-16.2±0.5)mV]향초급화방향이동료4.7 mV,차이유통계학의의(P<0.05); IS+CGRP조신경원개전류적반수실활전압V1/2위(-12.4±0.2) mV,교NS조[(-22.5±0.3)mY]향거겁화방향이동료10.1 mV,차이유통계학의의(P<0.05). 결론 격활경뇌막전입신경말소유도초급감각신경원적외주민화과정,돌출표현위개전류적증고.
Objective To investigate the modulation of sensitization of dural afferent nerve endings on high voltage active calcium currents (HVA-ICa) 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 (Va1/2) 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 current.