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去大脑猫小直径肌肉传入纤维化学诱导放电对γ-梭内肌运动神经元的反射效应。

Reflex effects on gamma fusimotor neurones of chemically induced discharges in small-diameter muscle afferents in decerebrate cats.

作者信息

Jovanović K, Anastasijević R, Vuco J

机构信息

Institute for Medical Research, Beograd, Yugoslavia.

出版信息

Brain Res. 1990 Jun 25;521(1-2):89-94. doi: 10.1016/0006-8993(90)91528-o.

Abstract

The effects on fusimotor discharge rate of algesic agents (bradykinin, potassium chloride, histamine, 5-hydroxytryptamine) and lactic acid, applied by close arterial injection into triceps surae muscles, were investigated in decerebrate cats. Fusimotor discharge was recorded from filaments dissected free from otherwise intact nerves to the triceps muscles. The substances applied induced an increase in discharge rate of spontaneously active gamma fusimotor neurones as well as a recruitment of previously silent ones. Skeletomotor discharges and/or muscle tension changes occurred only occasionally. The increase in fusimotor discharge rate was not always completely abolished by severing the nerves to triceps. What remained was a short-lasting burst at the very onset of blood-pressure fall. It was concluded that the increase in fusimotor discharge rate was mainly, but not solely, elicited reflexly by discharges from Group III and/or IV muscle afferents sensitive to algesic agents. An elevated fusimotor activity might be expected to accompany muscle inflammation and/or trauma when these agents are liberated in muscle tissue. The increase in fusimotor discharge rate elicited by lactic acid injections indicates that the fusimotor system might also be involved in neural processes of muscular fatigue.

摘要

在去大脑的猫身上,研究了通过向腓肠肌进行动脉内近距离注射痛觉介质(缓激肽、氯化钾、组胺、5-羟色胺)和乳酸对肌梭运动放电率的影响。从分离自完整的三头肌神经的细丝记录肌梭运动放电。所施加的物质会使自发活动的γ运动神经元的放电率增加,并且会使先前沉默的神经元开始放电。骨骼肌运动放电和/或肌肉张力变化只是偶尔发生。切断三头肌的神经并不总能完全消除肌梭运动放电率的增加。剩下的是血压下降刚开始时的一个短暂爆发。得出的结论是,肌梭运动放电率的增加主要(但并非唯一)是由对痛觉介质敏感的Ⅲ类和/或Ⅳ类肌肉传入纤维的放电反射性引起的。当这些介质在肌肉组织中释放时,预计在肌肉炎症和/或创伤时会伴随肌梭运动活动升高。乳酸注射引起的肌梭运动放电率增加表明,肌梭运动系统也可能参与肌肉疲劳的神经过程。

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