Effect of endogenous purines on electrically evoked ACh release at the mouse neuromuscular junction (original) (raw)

Journal of Neuroscience Research

Abstract

At the mouse neuromuscular junction, adenosine triphosphate (ATP), which is co‐released with the neurotransmitter acetylcholine (ACh), and its metabolite adenosine, modulate neurotransmitter release by activating presynaptic inhibitory P2Y13 receptors (a subtype of ATP/adenosine diphosphate [ADP] receptor), inhibitory A1 and A3 adenosine receptors, and excitatory A2A adenosine receptors. To study the effect of endogenous purines, when phrenic‐diaphragm preparations are depolarized by different nerve stimulation patterns, we analyzed the effect of the antagonists for P2Y13, A1, A3, and A2A receptors (AR‐C69931MX, 8‐cyclopentyl‐1,3‐dipropylxanthine, MRS‐1191, and SCH‐58261, respectively) on the amplitude of the end‐plate potentials of the trains, and contrasted these results with those obtained with the selective agonists of these receptors (2‐methylthioadenosine 5′‐diphosphate trisodium salt hydrate, 2‐chloro‐N6‐cyclopentyl‐adenosine, inosine, and PSB‐0777, respectively). During cont...

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