Baclofen blocks postsynaptic inhibition but not the effect of muscimol in the olfactory cortex

Abstract

1 The olfactory cortex slice preparation from the guinea-pig brain was used to study the effects of baclofen on inhibition using intracellular recording. Stimulation of the lateral olfactory tract activates sequentially excitatory and inhibitory pathways. Inhibition is manifest as a period of increased membrane conductance (termed postsynaptic inhibitory conductance, IPSC). 2 Bath application of baclofen (0.2–500 μm) reversibly blocked the IPSC. Baclofen also produced a secondary increase in the amplitude and duration of the initial excitatory postsynaptic potential. 3 Baclofen (0.5–500 μm) slightly augmented the ability of bath-applied muscimol to increase the resting membrane conductance. Baclofen had no effect on cell excitability and membrane potential and no effect on the action of γ-aminobutyric acid (GABA), noradrenaline, glycine, taurine or 5-hydroxytrypamine. 4 These results confirm previous suggestions that baclofen at low concentrations acts outside the GABA receptor mediating the IPSC perhaps by reducing the release of the excitatory transmitter activating the inhibitory interneurones.