The effect of reduced temperature on the inhibitory action of adenosine and magnesium ion at frog motor nerve terminals

A study was made to exclude the notion that adenosine receptor agonists exert a direct physical blockade of the depolarization‐secretion process. Reduced temperature was employed as a tool for distinguishing between physico‐chemical processes (such as those which mediate evoked transmitter release) and biochemical mechanisms (such as those which involve second messenger substances) in the action of adenosine. Adenosine and 2‐chloroadenosine were used as agonists in this electrophysiological study of the release of acetylcholine (ACh) from frog motor nerve terminals. The ability of these two adenosine receptor activators to reduce neurally‐evoked ACh release was prevented or greatly attenuated by maintaining the preparation at temperatures between 5 and 10°C. Such low temperatures inhibit the activation of receptors coupled to second messengers via guanine nucleotide binding proteins (e.g. adenylate cyclase). Low temperature alone did not substantially alter evoked ACh secretion under the conditions of these experiments. Inhibition of evoked ACh release by the extracellular Ca antagonist Mg, which acts directly to block Ca channels, was not affected by low temperature. The results are consistent with the hypothesis that a temperature‐sensitive second messenger system controls the intracellular events linked to extracellular adenosine receptor activation. 1988 British Pharmacological Society