Endogenous purines modulate K+ ‐evoked ACh secretion at the mouse neuromuscular junction

In conclusion, when motor nerve terminals are depolarized by increasing K+ concentrations, the ATP/ADP and adenosine endogenously generated are able to modulate ACh secretion by sequential activation of different purinergic receptors. At the mammalian neuromuscular junction, ATP is co‐released with the neurotransmitter ACh, and once in the synaptic cleft, it is hydrolyzed to adenosine. We report that, when motor nerve terminals are depolarized by increasing [K+]o, there is a sequence of activation of presynaptic purinergic receptors that are able to modulate neurosecretion.
Source: Journal of Neuroscience Research - Category: Neuroscience Authors: Tags: RESEARCH ARTICLE Source Type: research