COEXISTENCE OF PEPTIDES AND NEUROTRANSMITTERS

免疫组织化学研究显示降钙素基因- 运动细胞内CGRP与乙酰胆碱共存 脊髓损伤 因此，本研究旨在 研究胆碱能神经和 神经递质和CGRP对神经肌肉传递的影响 离体大鼠膈肌。 电刺激孤立的 膈神经引起抽搐收缩， 依赖性增强CGRP的浓度范围从 1.2 X 10-9 M至3 X 10-7 M。 CGRP（3）的增强作用 X 10 ~（-7）M）在25 min左右恢复到对照水平， 快速进化的 CGRP的作用依赖于 刺激脉冲宽度范围为0.2至1.0毫秒。 大鼠 降钙素（4.5 × 10-7 M）引起的最小变化， 抽搐收缩的幅度。 降钙素基因相关肽对 静止的横纹肌 对直流电的抽搐反应 CGRP（6 × 10 ~（-8）M - 6 × 10 ~（-7）M）也可增强刺激作用 在不存在和存在10-5 M d-筒箭毒碱的情况下。 这些 结果表明CGRP调节乙酰胆碱的作用 在横纹肌的运动终板处。 的可能性 神经末梢中正常肽含量的改变 （电机端板）的身体可能会导致各种肌肉 功能障碍具有重要的临床意义，应加以研究 在人类身上。

Immunohistochemical studies have revealed that calcitonin gene- related peptide (CGRP) coexists with acetylcholine in motor cells of the spinal cord. Therefore this study was undertaken to investigate a possible interaction between the cholinergic nerve neurotransmitter and CGRP on neuromuscular transmission in the isolated rat diaphragm. Electrical stimulation of the isolated phrenic nerve resulted in twitch contractions which were dose- dependently potentiated by CGRP in concentrations ranging from 1.2 X 10-9 M to 3 X 10-7 M. The potentiating action of CGRP (3 X 10-7 M) returned to control level in about 25 min and was rarely tachyphylactic. The action of CGRP was dependent upon the stimulation pulse width ranging from 0.2 to 1.0 msec. Rat calcitonin (4.5 X 10-7 M) caused a minimal change in the amplitude of twitch contractions. CGRP had no effect on the quiescent striated muscle. Twitch responses to direct electrical stimulation was also enhanced by CGRP (6 X 10-8 M - 6 X 10-7 M) in the absence and presence of 10-5 M d-tubocurarine. These results suggest that CGRP modulates the action of acetylcholine at the motor-end plates of striated muscle. The possibility that an alteration in the normal peptide content in nerve endings (motor-end plates) of the body may lead to a variety of muscle malfunctions is of great clinical significance and should be studied in humans.