MUSCLE HUSTLE: After stimulation with an action potential (1), the synaptic terminal of a motor neuron releases acetylcholine and ATP. (2) Acetylcholine activates receptors in the muscle, which spurs voltage-gated sodium channels to open, triggering an action potential in the muscle, which contracts. At the same time, ATP or ADP stimulates P2Y1 receptors (3), which causes calcium ions to be released from the endoplasmic reticulum of the terminal/perisynaptic Schwann cell (TPSC) (4). In response, perisynaptic potassium ions (K+) produced by the muscle and neuronal cells move into the TPSC (5). Regulation of perisynaptic potassium ions by TPSCs is thought to reduce the ions’ ability to inactivate voltage-gated sodium channels during repeated firing, thus reducing muscle fatigue.
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The paper
D.J. Heredia et al., “Activity-induced Ca2+ signaling in perisynaptic Schwann cells of the early postnatal mouse is mediated by P2Y1 receptors and regulates muscle fatigue,” eLife, 7:e30839, 2018.
At first glance, neurons and muscle cells are the stars of gross motor function. Muscle movement results from coordination between nerve and muscle cells: when an action potential arrives at the presynaptic neuron terminal, calcium ions flow, causing proteins to fuse with the cell membrane and release some of the neuron’s contents, including acetylcholine, into the cleft between the neuron and muscle cell. Acetylcholine binds to receptors on the muscle cell, sending calcium ions into it and causing it to contract.
But there’s also a third kind of cell at neuromuscular junctions, a terminal/perisynaptic Schwann cell ...
