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The Journal of Neuroscience, April 1, 1998, 18(7):2602-2612

Functional Organization of Rat Olfactory Bulb Glomeruli Revealed by Optical Imaging

Asaf Keller1, Sergey Yagodin1, Vassiliki Aroniadou-Anderjaska1, Lee A. Zimmer1, Matthew Ennis1, Norman F. Sheppard Jr2, and Michael T. Shipley1

1 Department of Anatomy and Neurobiology and the Program in Neuroscience, University of Maryland School of Medicine, Baltimore, Maryland 21201, and 2 Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland 21218 

The functional organization and synaptic physiology of olfactory bulb glomeruli were studied in rat in vitro slice preparations stained with the voltage-sensitive dye RH-155. Optical signals were recorded with a 100-element photodiode array at high temporal resolution. Pharmacological and ionic manipulations were used to investigate synaptic responses to stimulation of the olfactory nerve layer (ONL). ONL stimulation evoked a sodium-mediated compound action potential that propagated across the ONL and invaded individual glomeruli. This presynaptic volley evoked calcium-dependent synaptic responses the amplitudes of which were largest within the glomerular layer (GL); smaller amplitude responses were recorded in deeper layers of the olfactory bulb. Synaptic responses in the GL were attenuated by the non-NMDA ionotropic glutamate receptor antagonist CNQX; the residual component was suppressed by the NMDA glutamate receptor antagonist AP-5. The GABAA receptor antagonist bicuculline methiodide had little effect, whereas the GABAB receptor agonist baclofen dramatically attenuated ONL-evoked synaptic responses. The effects of baclofen were reversed by the GABAB receptor antagonist CGP35348. Paired-pulse depression of ONL-evoked synaptic responses in the GL was partially reversed by CGP35348. These findings suggest that olfactory nerve axons release glutamate to activate both NMDA and non-NMDA receptors on GL neurons, that GABAA receptor-mediated inhibition has little effect on these responses, and that GABAB receptor-mediated inhibition may act presynaptically on olfactory nerve axons to modulate their inputs to olfactory bulb neurons.

Key words: olfactory glomeruli; glutamate; NMDA; GABA; presynaptic inhibition; paired-pulse depression; CGP35348; RH-155


Copyright © 1998 Society for Neuroscience  0270-6474/98/1872602-11$05.00/0


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