Activity-induced Ca2+ signaling in perisynaptic Schwann cells is mediated by P2Y1 receptors and regulates muscle fatigue

摘要: Perisynaptic glial cells respond to neural activity by increasing cytosolic levels of calcium, but the functional significance this pathway is unclear. Terminal/persiynaptic Schwann (TPSCs) are a perisynaptic cell at neuromuscular junction. Here, we provide genetic evidence that activity-induced intracellular calcium accumulation in neonatal TPSCs mediated exclusively P2Y1 receptors. In P2ry1 mutant mice lacking these responses, postsynaptic, rather than presynaptic, function was altered response nerve stimulation. This impairment correlated with greater susceptibility muscle fatigue. Interestingly, fatigue mutants exacerbated exposure high potassium degree control mice. High itself increased TPSCs, which also reduced mutants. These results suggest responses glia NMJ regulate postsynaptic and influencing potassium.