Gabaergic control of odor-induced activity in the frog olfactory bulb: Electrophysiological study with picrotoxin and bicuculline

Abstract

In the olfactory bulb, the first relay of the olfactory pathways, GABA, could be largely involved in the information processing since the two main populations of interneurons, periglomerular and granular cells, use it as neurotransmitter through reciprocal synapses with second-order neurons. This study planned to clarify the role of GABAergic inhibition in odor coding and, more precisely, the role of glomerular GABAergic inhibition. To do so, we attempted to specifically block in vivo GABA A receptors with either picrotoxin or bicuculline. The drug was applied at the level of the glomerular layer so that the antagonist could act primarily via periglomerular cells. The analysis of the effects of blocking GABA A on the coding was studied by recording the second-order neuron responses to odor stimuli delivered in a wide concentration range. Under drug treatment, the second-order neuron properties were deeply changed: response thresholds to odors were often lowered and spike bursts were more sustained in frequency and in duration. Thus, the GABAergic control on second-order neurons might be carried out by limiting the neuron excitability. GABA A antagonists applied in this manner could act to suppress the inhibitory effect of either the periglomerular cells or of the granule cells, both of which have been shown to contain enzymes for GABA production. The placement of the drug suggests to us that the action is primarily at the glomerulus. The results are consistent with periglomerular cells exerting a tonic inhibition on second-order neurons, an inhibition whose strength would be modulated by stimulus intensity. As a result, the amplifying role of glomerular convergence might be partly counterbalanced by input inhibition. Nevertheless, due to our procedure of drug application, one cannot rule out the possibility that the effects observed may partly reflect granular cell blocking. It can be concluded that the whole GABAergic inhibition, through GABA A receptors, permits a wide dynamic range of intensity coding.