Modulation of transmitter release from the terminals of the locust wing stretch receptor neuron by muscarinic antagonists

Abstract

The forewing stretch receptor (SR) neuron makes monosynaptic connections with wing depressor motoneurons; in this article the pharmacology of its output onto the first basalar motoneuron (BA1) has been investigated. The SR, like other insect afferents that have been studied so far, appears to be cholinergic; transmission was suppressed reversibly by the nicotinic antagonist gallamine (10(-4) M) and irreversibly by alpha-bungarotoxin (10(-6) M). The choline reuptake blocker hemicholinium-3 (10(-4) M) also caused a reversible reduction in the amplitude of SR excitatory postsynaptic potentials (EPSPs) recorded in BA1. The receptor subtype nonselective muscarinic antagonists atropine (10(-4) M), scopolamine (10(-4) M), and quinuclidinyl benzilate (10(-5) M), unlike nicotinic antagonists, caused an augmentation in EPSP amplitude. This effect does not appear to be caused by an increase in sensitivity of the motoneuron to acetylcholine (ACh), since atropine produced a marked reduction rather than an increase in the amplitude of responses to ACh pressure applied to the soma of BA1. Scopolamine only caused a modest reduction in the amplitude of ACh somatic responses. The simplest explanation for these observations is that muscarinic antagonists bring about an increase in EPSP amplitude by blockade of presynaptic autoreceptors that normally down-regulate the release of ACh from SR terminals. The effects of muscarinic receptor subtype-selective antagonists indicate that presynaptic receptors in this preparation may have a pharmacological profile more similar to that of vertebrate M2 receptors than to that of M1 or M3 subtypes. The functional significance of autoreceptors in this preparation are discussed.