Calcitonin gene-related peptide prevents disuse-induced sprouting of rat motor nerve terminals
Calcitonin gene-related peptide prevents disuse-induced sprouting of rat motor nerve terminals
复制标题
降钙素基因相关肽可预防大鼠运动神经末梢废用性发芽
DOI：
10.1523/jneurosci.08-10-03951.1988
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发表时间：
1988
期刊：
影响因子：
9.9
通讯作者：
M. Kuno
中科院分区：
文献类型：
--
作者：
T. Tsujimoto;M. Kuno
降钙素基因相关肽（CGRP）与运动神经末梢中的乙酰胆碱（ACh）共存。外用 CGRP 已被证明可以通过独立于肌肉活动的机制增加培养的肌管中 ACh 受体的合成。因此，CGRP被认为是一种神经营养因子，可以调节神经肌肉接头处发生的几种长期事件的表达。我们研究了 CGRP 对成年大鼠神经肌肉活动慢性阻滞诱导的运动神经末梢萌发的影响。 CGRP 的每日治疗以剂量依赖性方式抑制废用诱导的末端萌芽，而活动肌肉中运动神经末梢的形态不受 CGRP 的影响。 CGRP 可能是抗芽剂的候选者，人们推测它存在于神经末梢中。废弃诱导的末端芽的生长伴随着终板电位的平均量子含量的增加，以及自发微型终板电位的频率的增加。这种增加的递质释放仍然维持在由 CGRP 抑制废用诱导的终末萌芽的连接处。有人认为，终端芽的形成本身并不是神经肌肉接头长期闲置引起的递质释放塑性变化的原因。
Calcitonin gene-related peptide (CGRP) coexists with acetylcholine (ACh) in motor nerve terminals. Externally applied CGRP has been shown to increase the synthesis of ACh receptors in cultured myotubes by a mechanism independent of muscle activity. Thus, CGRP is suggested to be a neurotrophic factor that may regulate the expression of several long- term events occurring at the neuromuscular junction. We have examined the effect of CGRP on the sprouting of motor nerve terminals induced by chronic block of nerve-muscle activity in adult rats. Daily treatment with CGRP suppressed the disuse-induced terminal sprouting in a dose- dependent manner, whereas the morphology of motor nerve terminals in active muscles was unaffected by CGRP. CGRP may be a possible candidate for an antisprouting agent which has been postulated to exist in nerve terminals. The disuse-induced outgrowth of terminal sprouts was accompanied by an increase in the mean quantum content of end-plate potentials, as well as in the frequency of spontaneous miniature end- plate potentials. This increased transmitter release was still maintained at the junctions in which disuse-induced terminal sprouting had been suppressed by CGRP. It is suggested that the formation of terminal sprouts per se is not responsible for the plastic change of transmitter release induced by prolonged disuse of the neuromuscular junction.