甲基丁香酚对吸气抑制性气道迷走节前神经元突触活动的影响  

Effects of methyleugenol on synaptic activities of inspiratory-inhibited airway vagal preganglionic neurons

作　　者：侯丽丽[1] 邱东鹰[2,3] 张旻[1] 张立清[4] 张杏怡[1] 李强[1] 周新[1] 

机构地区：[1]上海交通大学附属第一人民医院呼吸内科,上海200080 [2]复旦大学附属中山医院老年病科,上海200032 [3]复旦大学上海医学院生理与病理生理学系,上海200032 [4]山东省泰安荣军医院骨科,泰安271000

出　　处：《中国临床药学杂志》2017年第1期1-5,共5页Chinese Journal of Clinical Pharmacy

基　　金：国家自然科学基金(编号81300020)

摘　　要：目的探讨甲基丁香酚(MEG)对吸气抑制性气道迷走节前神经元(II-AVPNs)突触活动的影响。方法应用逆行荧光示踪技术,标记位于出生后3~5 d新生SD大鼠延髓疑核外侧区的气道迷走节前神经元(AVPNs);制备具有呼吸节律的离体延髓脑片;应用电生理学方法,记录舌下神经根的放电活动,鉴定II-AVPNs并记录其突触活动;向离体延髓脑片灌流100μmol·L^(-1)MEG,分别将应用MEG前后所记录的舌下神经根放电活动及II-AVPNs的突触活动分别作为对照组及MEG组。选择对照组最后10个、MEG组呼吸节律消失前5个呼吸周期连续的突触活动进行统计学分析。结果 100μmol·L^(-1)MEG能明显抑制II-AVPNs吸气期相位性外向电流(POC)及相位性抑制性突触后电流(IPSCs)。MEG组POC的幅度及面积分别为对照组的(46.37±6.74)%和(54.21±8.52)%,P均<0.001。MEG组吸气间期自发性IPSCs、兴奋性突触后电流(EPSCs)的频率及幅度明显低于对照组[(0.62±0.28)vs(2.36±0.66)Hz,(23.61±1.79)vs(27.43±1.42)p A;(4.73±0.84)vs(5.13±1.02)Hz;(25.09±2.63)vs(38.85±3.93)p A;P均<0.01]。结论 MEG通过抑制II-AVPNs吸气期相位性外向电流及兴奋性、抑制性突触活动来影响II-AVPNs的兴奋性。AIM To investigate the effects of methyleugenol （MEG） on synaptic activities of inspiratory-inhibited airway vagal preganglionic neurons （II-AVPNs）. METHODS AVPNs in the external formation （eNA） of 3 to 5-day-old SD rats were retrogradely labeled from the tracheal wall. The II-AVPNs were identified in rhythmically firing brainstem slices. The hypoglossal bursts and the synaptic activities of II-AVPNs were examined using electrophysiological methods. The hypoglossal bursts recorded from hypoglossal rootlets and synaptic activities of II- AVPNs prior to application of MEG were chosen as the control, and which during MEG application were considered as MEG group. The data from the last 10 consecutive inspiratory phases prior to application of MEG were analysed in the control, and the data from the last 5 respiratory cycles prior to rhythm blockade were used to represent the maximal effects of MEG group. RESULTS MEG （ 100 μmol·L-1） significantly inhibited inspiratory phasic outward current （POC） and phasic inhibitory postsynaptic currents （IPSCs）. Compared with the control, the amplitude and area of POC accounted for （46.37 ±6.74）% and （54.21±8.52）% （P〈0.001） respectively. The frequency and the amplitude of the spontaneous IPSCs during inspiratory bursts decreased [ （0.62 ±0.28）vs（2.36 ± 0.66） Hz, （23.61 ± 1.79）vs（27.43± 1.42） pA, all P 〈0. 001 ] during application of MEG. The frequency and amplitude of excitatory postsynaptic currents （EPSCs） during inspiratory bursts were also inhibited [ （4.73 ± 0.84）vs（5.13 ±1.02） Hz, P=0.01;（25.09±2.63）vs（38.85±3.93） pA, P〈0.001] in MEG group. CONCLUSION The results demonstrate that MEG affects the II-AVPNs via attenuation of POC and inhibition of inhibitory and excitatory synaptic inputs.

关 键 词：甲基丁香酚 迷走节前神经元 呼吸 突触传递 膜片钳技术 

分 类 号：R56[医药卫生—呼吸系统]