The physiology and pharmacology of the connections made by stress-sensitive campaniform sensilla on the proximal dorsal tibia of a locust hind leg with a fast extensor tibiae motor neuron (FETi) have been examined. 2. Mechanical stimulation of a campaniform sensillum on the anterior surface of the tibia elicited bursts of spikes in its afferent and a depolarization in FETi. Each afferent spike was followed at short and constant latency by an excitatory postsynaptic potential (EPSP) in FETi, even at high-frequency stimulation. Electrical stimulation of the extensor tibiae muscle with the tibia fixed elicited an antidromic spike in FETi followed by a compound potential which resulted from the activation of the campaniform sensillum afferent. The connections between the campaniform sensillum and FETi was monosynaptic and chemically mediated. 3. Ionophoresis of ACh into the neuropil depolarized FETi, as did the application of the cholinesterase inhibitor physostigmine. Bath application of the cholinergic agonists, nicotine and muscarine, also depolarized FETi, with nicotine causing a reduction in input resistance, while muscarine caused no detectable change in input resistance. Muscarine and the muscarinic agonist oxotremorine also caused rhythmic depolarizations and bursts of spikes in FETi. These effects were seen in low calcium/high magnesium saline to block synaptic transmission and are therefore due to direct effects on FETi. FETi therefore appears to have both nicotinic and muscarinic receptors. 4. The compound potential in FETi, caused by activation of the campaniform sensillum, was reduced by bath application of nicotinic cholinergic antagonists. However, the muscarinic antagonist scopolamine increased the amplitude of the compound potential.(ABSTRACT TRUNCATED AT 250 WORDS)
