The effect of gamma-aminobutyric acid (GABA) on synaptic transmission in rat superior cervical ganglion (SCG) was assessed in vitro by extracellular recording. Postganglionic compound action potentials (CAPs) triggered by preganglionic stimulation were blocked in a reversible and concentration-dependent fashion by short, 60 s long, superfusion with GABA (IC50 = 39.3 microM), with the GABAA agonist muscimol (IC50 = 8.7 microM) or with the GABAB agonist baclofen (IC50 = 145 microM). Responses to GABA and muscimol, but not to baclofen, exhibited desensitization after 5 min long superfusions with the drugs. In a long-term potentiation (LTP) paradigm, the degree of potentiation found 30 min after a tetanic train of stimuli (20 Hz for 20 s) was strongly inhibited by GABA (100-250 microM), when superfused at the time of tetanic stimulus or shortly thereafter. The effect of GABA on SCG LTP was mimicked by muscimol but not by baclofen. The results are compatible with the view that GABA exerts overall inhibitory effects in rat SCG, including transmission blockade of single impulses (through activation of GABAA and GABAB receptors) and impairment of activity-dependent potentiation of nicotinic transmission (through activation of GABAA receptors).