Role of ganglionic cotransmission in sympathetic control of the isolated bullfrog aorta.
Role of ganglionic cotransmission in sympathetic control of the isolated bullfrog aorta.
复制标题
神经节共传递在离体牛蛙主动脉交感神经控制中的作用。
DOI：
10.1113/jphysiol.1997.sp021851
复制
发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Horn,JP
中科院分区：
文献类型：
--
作者：
Thorne,R;Horn,JP
1. 在制备牛蛙腰交感神经节7‐10和背主动脉时，研究了节前活动与动脉张力的关系。2. 当两个或两个以上的刺激作用于神经节前C通路时，会引起收缩，但B通路则不会。当切断交感神经链或加入（+）‐管碱阻断第9节和第10节的传导时，收缩被阻断。节后作用的胍乙啶可拮抗收缩，而酚妥拉明或苏拉明则不能。3. 主动脉对短脉冲（10 - 100次刺激）的反应在0.3 - 0.5 Hz时达到一半最大，在1hz附近达到饱和，最小潜伏期为8.9 s。相比之下，对300个刺激的反应在1hz时是最大反应的一半，在10hz时是最大反应的2.5倍。外源性黄体生成素释放激素（LHRH）增强了神经节前诱发的收缩。内源性LHRH介导的（+）‐管curarine 10hz刺激引起的收缩。这些反应具有比正常林格溶液更长的潜伏期，并且被[D‐pGlu1， D‐Phe2, D‐Trp3.6]‐LHRH阻断。LHRH拮抗剂不改变正常林格氏液持续刺激或六甲溴铵刺激引起的收缩。5. 外源性神经肽Y （NPY）增强神经源性收缩和对肾上腺素的反应。苯特拉明能阻断神经刺激、肾上腺素和NPY引起的收缩，但不能阻断ATP。6. 结果表明，离体主动脉的收缩与交感C神经元活动的生理频率一致。神经节中的肽能共传递可以增加动脉张力，但在初级尼古丁突触的同步激活期间不会增加。这表明LHRH的生理作用来自于与阈下尼古丁epsp的相互作用，以及神经节后NPY的释放在长时间活动期间改变了电路的频率调谐。
1. The relation between preganglionic activity and arterial tone was studied in preparations of bullfrog lumbar sympathetic ganglia 7‐10 and the dorsal aorta. 2. Two or more stimuli evoked contractions when applied to the preganglionic C, but not the B pathway. Contractions were blocked when transmission in ganglia 9 and 10 was disrupted by cutting the sympathetic chain or adding (+)‐tubocurarine. Contractions were antagonized by postganglionic action of guanethidine, but not by phentolamine or suramin. 3. Aortic responses to short trains (10‐100 stimuli) were half‐maximal at 0.3‐0.5 Hz, saturated near 1 Hz and had a minimum latency of 8.9 s. By contrast, responses to 300 stimuli were half‐maximal at 1 Hz and became 2.5‐fold larger at 10 Hz. 4. Exogenous luteinizing hormone releasing hormone (LHRH) potentiated preganglionically evoked contractions. Endogenous LHRH mediated contractions evoked by 10 Hz stimulation in (+)‐tubocurarine. These responses had a longer latency than in normal Ringer solution and were blocked by [D‐pGlu1, D‐Phe2, D‐Trp3.6]‐LHRH. The LHRH antagonist did not alter contractions evoked by continuous stimulation in normal Ringer solution or by bursts of stimuli in hexamethonium. 5. Exogenous neuropeptide Y (NPY) potentiated neurogenic contractions and responses to adrenaline. Benextramine blocked contractions produced by nerve stimulation, adrenaline and NPY, but not ATP. 6. The results show that contractions of the isolated aorta are tuned to physiological frequencies of activity in sympathetic C neurones. Peptidergic cotransmission in the ganglia can increase arterial tension, but not during synchronous activation of primary nicotinic synapses. It is suggested that the physiological role of LHRH arises from interactions with subthreshold nicotinic EPSPs and that postganglionic release of NPY shifts frequency tuning of the circuit during prolonged activity.