EVIDENCE FOR GABA(B)-MEDIATED INHIBITION OF TRANSMISSION FROM THE OLFACTORY NERVE TO MITRAL CELLS IN THE RAT OLFACTORY-BULB

The GABA(B) agonist baclofen blocks transmission from the olfactory ne rve to second order neurons in the frog olfactory bulb, and GABA(B) re ceptors in the rat olfactory bulb are selectively located in the glome rular layer. A reasonable hypothesis, therefore, is that inhibition in the glomerular layer is mediated, at least in part, by GABA(B) recept ors. Here, we investigated the role of GABA(B) receptors in regulating the responses of mitral cells to activation of the olfactory nerve in the rat. Topical application of baclofen to the surface of the rat ol factory bulb reduced the amplitude of field potentials evoked by olfac tory nerve stimulation (orthodromic response). Baclofen reduced the or thodromic response in a dose-dependent manner but the drug had no effe ct on the field potential evoked by antidromic activation of mitral ce ll axons (antidromic response). Baclofen also reduced olfactory nerve- evoked responses of mitral cells in an olfactory bulb slice preparatio n. The pharmacological specificity of the inhibition was confirmed by showing that the GABA(B) antagonist, CGP 55845A, blocked the inhibitor y action of baclofen. These results suggest that transmission from olf actory nerve terminals to second order neurons is negatively regulated by periglomerular GABAergic interneurons; this inhibition is mediated , at least partially, by GABA(B) receptors.