Transduction mechanism involving the presynaptic adenosine receptor at mouse motor nerve terminals.

The inhibitory effect of 2-chloroadenosine on spontaneous quantal release of transmitter at the mouse neuromuscular junction was abolished after pretreating tissues either with pertussis toxin (PTX), or with H7, a protein kinase inhibitor. H7 alone caused a fall in miniature endplate potential (MEPP) frequency, but PTX did not. The results are consistent with the hypothesis that rates of neurotransmitter release are directly related to intraterminal cyclic AMP levels, and that these can be reduced by A1 adenosine receptor agonists through the mediation of a Gi protein.