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Neural regulation of acetylcholine receptors in rat neonatal muscle.

机译:大鼠新生肌肉中乙酰胆碱受体的神经调节。

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摘要

1. The neuronal regulation of the developmental decline in skeletal muscle acetylcholine (ACh) receptors was studied by comparing the effects of sciatic nerve section or of neuromuscular blockade with botulinum toxin (BoTX) on this decline in neonatal and adult rats, using 125I-alpha-bungarotoxin (125I-BTX) as a ligand for the receptor alpha-subunit. 2. The decline in 125I-BTX binding site concentration in neonatal rat triceps surae muscle homogenates towards low, adult levels followed a simple exponential with a time constant of 8 days. This decline occurred while the muscle is still rapidly growing, before the postnatal increase in numbers of sodium channels. It also preceded the decline in muscle ACh receptor alpha-subunit mRNA, reported in other studies, suggesting that subunit levels are not regulated only by mRNA availability. 3. Muscle denervation in the first two weeks of life prevented this developmental decline. Denervation increased the concentration of 125I-BTX binding sites but the magnitude of this increase became progressively smaller as the muscle matured, showing that removal of innervation during adult life does not revert the muscle, in toto, to its pre-innervation state. 4. Blockade of neuromuscular activity with BoTX increased 125I-BTX binding sites to a lesser extent than muscle denervation during neonatal life. This lesser effect of BoTX blockade contrasts with the equal effects of BoTX blockade and denervation in the adult.
机译:1.通过使用125I-alpha比较坐骨神经切片或神经肌肉阻滞与肉毒杆菌毒素(BoTX)对新生和成年大鼠的这种下降的影响,研究了骨骼肌乙酰胆碱(ACh)受体发育下降的神经元调节作用。 -bungarotoxin(125I-BTX)作为受体α-亚基的配体。 2.新生大鼠肱三头肌腓肠肌中125 I-BTX结合位点浓度的下降趋向于低的成年水平,遵循简单的指数,时间常数为8天。这种下降发生在肌肉仍迅速生长的时候,而在出生后钠通道数量增加之前。在其他研究中也报道了肌肉ACh受体α亚基mRNA下降之前,这表明亚基水平不仅受mRNA可用性的调节。 3.生命的前两周肌肉神经支配防止了这种发育下降。去神经作用增加了125I-BTX结合位点的浓度,但是随着肌肉的成熟,这种增加的幅度逐渐变小,这表明在成年生活中去除神经支配不会使肌肉恢复到其神经支配前的状态。 4.在新生儿生命中,用BoTX阻断神经肌肉活动增加了125I-BTX结合位点,其程度小于肌肉神经支配。 BoTX封锁的这种较小影响与成人中BoTX封锁和神经支配的同等作用形成对比。

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