Effects of goniopora toxin on non‐adrenergic, non‐cholinergic response and purine nucleotide release in guinea‐pig taenia coli

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Abstract
Effects of goniopora toxin (GPT) on nonadrenergic, noncholinergic inhibitory responses were examined in isolated guinea pig tenia coli and the transmission mechanism was analyzed. GPT (20-50 nM) gradually augmented the relaxation and rebound contraction induced by electrical transmural stimulation in the presence of guanethidine and atropine. These effects were abolished by tetrodotoxin. The resting tension and the response to exogenously applied ATP were little affected by GPT. The action potentials and the electrotonic potentials recorded by a double sucrose-gap method were little affected by GPT. The augmentation was elicited by a direct action of GPT on the nonadrenergic, noncholinergic neurons, rather than on the smooth muscles. GPT augmented the amplitude of the inhibitory junction potential (IJP) recorded in the presence of guanethidine and atropine. GPT also enhanced the 3H efflux in response to electrical transmural stimulation of preparations preloaded with [3H]adenosine. Tetrodotoxin markedly inhibited or abolished the IJP and 3H efflux. Augmentation of the nonadrenergic, noncholinergic responses was due to increased transmitter release from the nerve. Under conditions in which the transmitter release was augmented, the nonadrenergic, noncholinergic response showed an essentially similar pattern to that obtained under normal conditions. The inhibitory response was probably due to a putative transmitter, possibly ATP or a related nucleotide.