We investigated the involvement of GABA-A receptors in the modulation of the nicotinic transmission of central origin in isolated rabbit coeliac ganglia. Our study was performed in vitro and the electrical activity of the ganglionic neurones was recorded using intracellular recording techniques. During iterative stimulation of the splanchnic nerves, the synaptic action potential probability decreased gradually, indicating a depression of the nicotinic activation. Pharmacological agents acting at GABA-A receptors modulated the action potential probability during the train of pulses. Muscimol (a GABA-A receptor agonist), diazepam (a benzodiazepine site agonist) and 1-[2-[[(diphenylmethylene)imino]oxy]ethyl]-1,2,5,6-tetrahydro-3-pyridinecarboxylic acid hydrochloride (a GABA uptake blocker) increased this probability. Conversely, gabazine or bicuculline (two GABA-A receptor antagonists), picrotoxin (a picrotoxin site agonist) and flumazenil (a benzodiazepine site antagonist) reduced it. These results demonstrate that endogenous GABA, released during the train of pulses, facilitates the central nicotinic activation of the ganglionic neurones by acting on GABA-A receptors. Muscimol also reduced the amplitude ratio of excitatory postsynaptic potentials triggered during the paired-pulse protocol without any change in postsynaptic properties. This result is consistent with a presynaptic action of GABA-A receptors. Our study shows that presynaptic GABA-A receptors facilitate the central nicotinic activation of prevertebral ganglionic neurones and thus play a novel role in the integrative properties of the sympathetic prevertebral ganglia.