Effect of γ-aminobutyric acid on synaptic transmission and long-term potentiation in rat superior cervical ganglion

Abstract

The effect of γ-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 (IC 50 = 39.3 μM), with the GABA A agonist muscimol (IC 50 = 8.7 μM) or with the GABA B agonist baclofen (IC 50 = 145 μM). 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 μM), 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 GABA A and GABA B receptors) and impairment of activity-dependent potentiation of nicotinic transmission (through activation of GABA A receptors).