Presynaptic inhibition is mediated by histamine and GABA in the crustacean escape reaction.

1. Presynaptic inhibition of sensory transmission during the escape reaction in Crustacea has been studied using an in vitro preparation of the crayfish thoracic ganglia. Electrical stimulation of the medial giant fiber mediating the escape reaction induced depolarization in sensory afferent terminals of the coxo-basal chordotonal organ (CBCO). This depolarization was associated with an increase of the membrane conductance and was partially blocked by a gamma-aminobutyric acid (GABA) antagonist, picrotoxin, and by a histamine antagonist, cimetidine. 2. Pressure ejection of histamine on CBCO sensory terminals (CBT) recorded intracellularly, induced a depolarization of the membrane potential accompanied by a large increase of the conductance. Histamine-induced depolarization persisted after blockade of synaptic transmission mediated by Na+ spikes by tetrodotoxin. The amplitude of histamine-induced depolarization increased when negative current was injected into the sensory terminal through the recording electrode. Moreover, injection of chloride into the CBT, which shifts the reversal potential of chloride to a more positive value, resulted in an increase of the amplitude of the histamine-induced depolarization. 3. The existence of separate receptors for GABA and histamine on the CB sensory terminals was demonstrated using two complementary sets of experiments. The first one consisted of using specific blockers of GABA and histamine. Picrotoxin blocked selectively the GABA-induced depolarization of the CB sensory terminals, while it was ineffective in blocking the histamine-induced depolarization. Conversely, cimetidine blocked the histamine-induced depolarization totally, but did not affect the GABA response. The second set of experiments tested for of cross-desensitization between GABA and histamine responses.(ABSTRACT TRUNCATED AT 250 WORDS)