GABA(B)-mediated action in the frog olfactory bulb makes odor responses more salient

In the olfactory bulb, GABA(B) receptors are selectively located in the glo merular layer. A current hypothesis is that GABAergic inhibition mediated t hrough these receptors would be, at least partly, presynaptic and would exe rted by decreasing the release of the olfactory receptor neuron excitatory neurotransmitter. Here, we assessed, in the frog, the in vivo action of bac lofen, a GABA(B) agonist, on single-unit mitral cell activity in response t o odors. Local application of baclofen in the glomerular region of the olfa ctory bulb was shown to drastically affect mitral cell spontaneous activity , since they became totally silent. Moreover, under baclofen, mitral cells still responded to odors and still specified odor concentration increases t hrough their temporal response patterns. The pharmacological specificity of the GABA(B) agonist action was confirmed by showing that saclofen, a GABA( B) antagonist, partly prevented the inhibitory action of baclofen and resto red the initial rate of mitral cell spontaneous activity. The results show that GABA(B)-mimicked inhibition suppressed mitral cell sp ontaneous activity while odor responses were maintained. This suggests that olfactory receptor neurons partly drive spontaneous mitral cell activity. Moreover, the effect of GABA(B)-mediated inhibition was seen to be very clo se to that described previously for dopamine D-2 receptor-mediated inhibiti on. In conclusion, we propose that these two inhibitory mechanisms would of fer the possibility to reduce or suppress mitral cell spontaneous activity so as to make their responses to odor especially salient. (C) 2000 IBRO. Pu blished by Elsevier Science Ltd.