中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2015年
12期
933-937
,共5页
侯丽丽%周新%张旻%刘振威%张国清
侯麗麗%週新%張旻%劉振威%張國清
후려려%주신%장민%류진위%장국청
丁香酚%迷走神经%呼吸%突触传递%膜片钳技术
丁香酚%迷走神經%呼吸%突觸傳遞%膜片鉗技術
정향분%미주신경%호흡%돌촉전체%막편겸기술
Eugenol%Vagus Nerve%Respiration%Synaptic Transmission%Patch-Clamp Techniques
目的 探讨甲基丁香酚对气道迷走节前神经元(AVPNs)中枢性呼吸驱动的影响.方法 应用逆行荧光示踪技术,标记3～5d新生SD大鼠疑核腹外侧区的吸气激活性-气道迷走节前神经元(IA-AVPNs);制备具有呼吸节律的离体延髓脑片,记录舌下神经根放电活动;应用膜片钳技术,记录IA-AVPNs的兴奋性突触活动.将脑片分为应用甲基丁香酚前的对照组及应用甲基丁香酚的甲基丁香酚组.选择对照组最后10个、甲基丁香酚组呼吸节律消失前5个呼吸周期连续的舌下神经根放电及对应的兴奋性突触活动进行统计学分析.结果 甲基丁香酚组舌下神经根放电的频率、幅度、时程及面积显著低于对照组[(2.14±0.87)次/min、(1.27±0.53) mV、(178±37) ms、(330±173) mV· ms比(5.39±1.93)次/min、(2.94 ±0.92)mV、(249±54) ms、(983±534) mV· ms,均P＜0.001],IA-AVPNs吸气期相位性内向电流的幅度、时程及面积分别为对照组的(66.3±4.4)％、(58.5±4.3)％、(44.9±7.5)％(均P ＜0.05),IA-AVPNs吸气期相位性兴奋性突触后电流(EPSCs)的频率显著低于对照组[(29.87±3.70)比(42.27±11.95) Hz]、但幅度显著高于对照组[(83.13±15.97)比(49.26 ±7.40) pA](均P＜0.05);两组IA-AVPNs吸气间期紧张性的EPSCs频率及幅度差异均无统计学意义(均P ＞0.05).结论 甲基丁香酚通过抑制IA-AVPNs吸气期兴奋性突触传入抑制IA-AVPNs的中枢性呼吸驱动.
目的 探討甲基丁香酚對氣道迷走節前神經元(AVPNs)中樞性呼吸驅動的影響.方法 應用逆行熒光示蹤技術,標記3～5d新生SD大鼠疑覈腹外側區的吸氣激活性-氣道迷走節前神經元(IA-AVPNs);製備具有呼吸節律的離體延髓腦片,記錄舌下神經根放電活動;應用膜片鉗技術,記錄IA-AVPNs的興奮性突觸活動.將腦片分為應用甲基丁香酚前的對照組及應用甲基丁香酚的甲基丁香酚組.選擇對照組最後10箇、甲基丁香酚組呼吸節律消失前5箇呼吸週期連續的舌下神經根放電及對應的興奮性突觸活動進行統計學分析.結果 甲基丁香酚組舌下神經根放電的頻率、幅度、時程及麵積顯著低于對照組[(2.14±0.87)次/min、(1.27±0.53) mV、(178±37) ms、(330±173) mV· ms比(5.39±1.93)次/min、(2.94 ±0.92)mV、(249±54) ms、(983±534) mV· ms,均P＜0.001],IA-AVPNs吸氣期相位性內嚮電流的幅度、時程及麵積分彆為對照組的(66.3±4.4)％、(58.5±4.3)％、(44.9±7.5)％(均P ＜0.05),IA-AVPNs吸氣期相位性興奮性突觸後電流(EPSCs)的頻率顯著低于對照組[(29.87±3.70)比(42.27±11.95) Hz]、但幅度顯著高于對照組[(83.13±15.97)比(49.26 ±7.40) pA](均P＜0.05);兩組IA-AVPNs吸氣間期緊張性的EPSCs頻率及幅度差異均無統計學意義(均P ＞0.05).結論 甲基丁香酚通過抑製IA-AVPNs吸氣期興奮性突觸傳入抑製IA-AVPNs的中樞性呼吸驅動.
목적 탐토갑기정향분대기도미주절전신경원(AVPNs)중추성호흡구동적영향.방법 응용역행형광시종기술,표기3～5d신생SD대서의핵복외측구적흡기격활성-기도미주절전신경원(IA-AVPNs);제비구유호흡절률적리체연수뇌편,기록설하신경근방전활동;응용막편겸기술,기록IA-AVPNs적흥강성돌촉활동.장뇌편분위응용갑기정향분전적대조조급응용갑기정향분적갑기정향분조.선택대조조최후10개、갑기정향분조호흡절률소실전5개호흡주기련속적설하신경근방전급대응적흥강성돌촉활동진행통계학분석.결과 갑기정향분조설하신경근방전적빈솔、폭도、시정급면적현저저우대조조[(2.14±0.87)차/min、(1.27±0.53) mV、(178±37) ms、(330±173) mV· ms비(5.39±1.93)차/min、(2.94 ±0.92)mV、(249±54) ms、(983±534) mV· ms,균P＜0.001],IA-AVPNs흡기기상위성내향전류적폭도、시정급면적분별위대조조적(66.3±4.4)％、(58.5±4.3)％、(44.9±7.5)％(균P ＜0.05),IA-AVPNs흡기기상위성흥강성돌촉후전류(EPSCs)적빈솔현저저우대조조[(29.87±3.70)비(42.27±11.95) Hz]、단폭도현저고우대조조[(83.13±15.97)비(49.26 ±7.40) pA](균P＜0.05);량조IA-AVPNs흡기간기긴장성적EPSCs빈솔급폭도차이균무통계학의의(균P ＞0.05).결론 갑기정향분통과억제IA-AVPNs흡기기흥강성돌촉전입억제IA-AVPNs적중추성호흡구동.
Objective To explore the effects of methyleugenol (MEG) on central respiratory drive to inspiratory-activated airway vagal preganglionic neurons (IA-AVPNs).Methods The 3 to 5-day-old Sprague-Dawley rats were anesthetized and rhodamine was injected into trachea wall for labelling IA-AVPNs in ventrolateral vicinity of nucleus ambiguous (vNA).And then a brainstem slice preparation with hypoglossal rootlets was made.IA-AVPNs were identified and excitatory synaptic inputs were recorded with patch-clamp techniques.Brainstem slice preparations were divided into the groups of control prior to application of MEG and MEG during MEG application.The data from the last 10 consecutive inspiratory phases prior to application of MEG were chosen as control.And the data from the last 5 respiratory cycles prior to rhythm blockade were used to represent the maximal effects of MEG group.Paired Student's t-test was used for comparing inter-group differences.Results Compared with control,MEG group had lower frequency,amplitude,duration and area of hypoglossal bursts (2.14 ± 0.87 vs 5.39 ± 1.93 burst/min,1.27 ±0.53 vs 2.94 ± 0.92 mV,178 ± 37 vs 249 ± 54 ms,330 ± 173 vs 983 ± 534 mV · ms,all P ＜ 0.001).The duration,amplitude and area of phasic inspiratory inward current were lower in MEG group,accounting for (66.3 ± 4.4) ％,(58.5 ± 4.3) ％,(44.9 ± 7.5) ％ (all P ＜ 0.05) of control respectively.Compared with control,the frequency of phasic excitatory postsynaptic currents (EPSCs) was lower (29.87 ±3.70 vs 42.27 ± 11.95 Hz) during inspiratory bursts but the amplitude was higher (83.13 ± 15.97 vs 49.26 ± 7.40 pA) (all P ＜ 0.05).However,compared with control,no significant differences existed in the frequency and amplitude of tonic EPSCs during inspiratory intervals (all P ＞ 0.05).Conclusion MEG inhibits central respiratory drive to IA-AVPNs through inhibiting excitatory synaptic transmission.
