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The Journal of Neuroscience, June 1, 2001, 21(11):3819-3829

Synapse-Glia Interactions at the Mammalian Neuromuscular Junction

Danielle Rochon, Isabelle Rousse, and Richard Robitaille

Centre de Recherche en Sciences Neurologiques and Département de Physiologie, Université de Montréal, Montréal, Quebec, Canada H3C 3J7

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 as 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 -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.

Key words: adenosine; acetylcholine; Ca²⁺; perisynaptic Schwann cell; transmitter release; neuromuscular junction; synapse-glia interactions

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Copyright © 2001 Society for Neuroscience  0270-6474/01/21113819-11$05.00/0

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