Synapse-glia interactions at the mammalian neuromuscular junction
Synapse-glia interactions at the mammalian neuromuscular junction
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DOI：
10.1523/jneurosci.21-11-03819.2001
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发表时间：
2001-06-01
影响因子：
5.3
通讯作者：
Robitaille, R
中科院分区：
文献类型：
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作者：
Rochon, D;Rousse, I;Robitaille, R
突触周雪旺细胞（PSC）在调节和稳定哺乳动物神经肌肉接头（NMJ）的神经末梢中起着关键作用。然而，尽管这些功能可能是由突触特性调节的，但PSC与突触元件的相互作用尚不清楚。因此，我们的目标是研究哺乳动物PSC在原位和突触前末梢之间的相互作用，使用细胞内Ca 2+的变化作为细胞活性的指标。运动神经刺激可引起PSC细胞内Ca ~（2+）浓度升高，当阻断递质释放时，这种升高大大降低。此外，局部应用乙酰胆碱诱导的Ca 2+的反应，被阻断的毒蕈碱拮抗剂阿托品和模仿的毒蕈碱激动剂毒蕈碱。烟碱拮抗剂α-银环蛇毒素对乙酰胆碱诱导的Ca ~（2+）反应无影响。局部应用协同递质ATP诱导的Ca 2+反应不受P2受体拮抗剂苏拉明的影响，而局部应用腺苷诱导的Ca 2+反应则被A1受体拮抗剂8-环戊基-1，3-二甲基黄嘌呤（CPT）大大降低。然而，在灌流液中的A1拮抗剂的存在下，不阻断ATP诱导的反应。在CPT的存在下，由刺激运动神经引起的Ca 2+反应减少，而阿托品几乎完全消除它们。当两种拮抗剂同时存在时，Ca 2+反应进一步降低。因此，哺乳动物NMJ处的PSC通过激活毒蕈碱和腺苷A1受体对由运动神经刺激诱导的神经递质的释放做出响应。
Perisynaptic Schwann cells (PSCs) play critical roles in regulating and stabilizing nerve terminals at the mammalian neuromuscular junction (NMJ). However, although these functions are likely regulated by the synaptic properties, the interactions of PSCs with the synaptic elements are not known. Therefore, our goal was to study the interactions between mammalian PSCs in situ and the presynaptic terminals using changes in intracellular Ca2+ as an indicator of cell activity. Motor nerve stimulation induced an increase in intracellular Ca2+ in PSCs, and this increase yas greatly reduced when transmitter release was blocked. Furthermore, local application of acetylcholine induced Ca2+ responses that were blocked by the muscarinic antagonist atropine and mimicked by the muscarinic agonist muscarine. The nicotinic antagonist alpha -bungarotoxin had no effect on Ca2+ responses induced by acetylcholine. Local application of the cotransmitter ATP induced Ca2+ responses that were unaffected by the P2 antagonist suramin, whereas local application of adenosine induced Ca2+ responses that were greatly reduced by the A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT). However, the presence of the A1 antagonist in the perfusate did not block responses induced by ATP. Ca2+ responses evoked by stimulation of the motor nerve were reduced in the presence of CPT, whereas atropine almost completely abolished them. Ca2+ responses were further reduced when both antagonists were present simultaneously. Hence, PSCs at the mammalian NMJ respond to the release of neurotransmitter induced by stimulation of the motor nerve through the activation of muscarinic and adenosine A1 receptors.