GABA, the major inhibitory neurotransmitter involved in information processing in the olfactory bulb, is hypothesized to act through GABA(B) receptors by depressing primary neurotransmitter release at the level of olfactory nerve axon endings. The present study was designed to analyze GABA(B) receptor-mediated inhibition mechanisms by performing whole-cell patch-clamp recordings of mitral/tufted cell activity in the rat in vitro. To do so, GABA(B) receptor-mediated action was mimicked by baclofen and antagonized by saclofen. Our protocol led us to provide an original description of GABA(B) receptor-mediated inhibition exerted on mitral/tufted cells. First, their spontaneous activity was shown to be drastically abolished by baclofen. Second, their responses to olfactory nerve electrical stimulation were graded by GABA(B) receptor-mediated inhibition. Indeed, this inhibition may be described as inducing effects ranked from a slight increase in response latency to a complete response suppression.Altogether, our results corroborate the hypothesis of a presynaptic extrasynaptic GABA(B) receptor-mediated inhibition influencing mitral/tufted cell olfactory nerve responsivity. However, the involvement of postsynaptic receptors, with different properties or with different anatomical locations, cannot be ruled out, particularly in the control of spontaneous activity. In conclusion, we underline that, in the vertebrate olfactory bulb, GABA(B) receptor-mediated action appears to contribute to make mitral/tufted cell responses more salient by reducing their resting activity.