Abstract

The ability of humoral agonists (and their persistent analogues) to induce contractions of denervated m. soleus and m. extensor digitorum longus of mice was investigated. Earlier, we found a change in the effectiveness of the ATP modulating effect under some non-physiological factors in the neuromuscular synapses of rodents. The aim of this study was to evaluate the effect of ATP on the contractility of isolated skeletal muscles of a mouse after traumatic denervation. It has been shown that 28-day denervation led to an increase in the strength of contractions of m. soleus and m. extensor digitorum longus caused by an acetylcholine analog. ATP application induced a contraction of denervated muscles, but not of intact ones. In the presence of a non-selective P2 receptor antagonist suramin, the effect of ATP ceased. We suggest that activation of postsynaptic P2X receptors of denervated muscles could cause their contraction. Apparently, this effect was caused by an increase in the expression of postsynaptic receptors in response to a violation of neurotrophic control and the conductive ability of the nerve fiber.

中文翻译：

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ATP 导致失神经骨骼肌收缩

摘要

体液激动剂（及其持久类似物）诱导去神经肌收缩的能力。比目鱼和m。 研究了小鼠的趾长伸肌。此前，我们发现啮齿动物神经肌肉突触在一些非生理因素作用下，ATP调节作用的有效性发生了变化。本研究的目的是评估 ATP 对创伤性去神经术后小鼠离体骨骼肌收缩力的影响。研究表明，28 天的去神经支配导致 m 收缩强度增加。比目鱼和m。由乙酰胆碱类似物引起的趾长伸肌。ATP 的应用会引起去神经肌肉的收缩，但不会引起完整肌肉的收缩。在存在非选择性 P2 受体拮抗剂苏拉明的情况下，ATP 的作用停止。我们认为去神经支配肌肉的突触后 P2X 受体的激活可能导致其收缩。显然，这种效应是由于神经营养控制和神经纤维传导能力受到破坏而导致突触后受体表达增加所致。