COEXISTENCE OF PEPTIDES AND NEUROTRANSMITTERS

免疫组织化学研究表明，降钙素基因- 运动细胞中相关肽(CGRP)与乙酰胆碱共存 脊髓的损伤。因此，这项研究是为了 研究胆碱能神经之间可能的相互作用 神经递质和降钙素基因相关肽对大鼠神经肌肉传递的影响 分离的大鼠横隔膜。孤立性的电刺激 膈神经引起抽搐收缩，其剂量- 依赖于由CGRP在以下浓度范围内增强 1.2×10~(-9)M~3×10~(-7)M。CGRP(3)的增强作用 X 10-7M)在大约25分钟内恢复到控制水平，并且很少 迟发性窒息。降钙素基因相关肽的作用依赖于 刺激脉冲宽度为0.2-1.0毫秒。大鼠 降钙素(4.5×10~(-7)M)对 抽搐收缩的幅度。降钙素基因相关肽对大鼠心脏功能无明显影响。 静止的横纹肌。对直流电的抽动反应 CGRP(6×10~(-8)M~(-6)×10~(-7)M)也能增强刺激作用。 在10~(-5)M-D-管胡萝卜碱存在和不存在的情况下。这些 结果提示CGRP对乙酰胆碱的作用有调节作用。 在横纹肌的运动终板上。有没有可能 神经末梢正常多肽含量的变化 身体的(运动终板)可能导致多种肌肉 故障具有重要的临床意义，值得研究。 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.