Octopamine release has been demonstrated from the dorsal unpaired median neurone to the locust extensor-tibiae muscle (DUMETi) in response to high-[K+] saline. Here, we provide evidence for the existence of presynaptic inhibitory autoreceptors for octopamine on the DUMETi terminals and report on their pharmacological profile. Octopamine release was initiated by exposure to high-[K+] saline (0. 1 mol l-1) and measured using a radioenzyme assay for octopamine. Octopamine receptor antagonists (10(-4 )mol l-1) potentiated the high-[K+]-mediated release of octopamine with the following rank order of potency: phentolamine = metoclopramide > mianserin = chlorpromazine > cyproheptadine > yohimbine. Octopamine receptor agonists (10(-4 )mol l-1) inhibited the high-[K+]-mediated release of octopamine with the following rank order of potency: naphazoline > tolazoline > clonidine. Thus, the octopamine autoreceptors on the DUMETi terminals are much closer pharmacologically to the pre-and postsynaptic OCTOPAMINE2 receptors in the locust extensor-tibiae muscle preparation than to the OCTOPAMINE3 receptors from the locust central nervous system. The results suggest that there is likely to be more than one type of insect neuronal octopamine receptor. It is also likely that presynaptic modulation of octopamine release may be confined to octopamine receptors since a wide range of other putative modulatory substances did not produce this effect.

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