Artigo Acesso aberto Revisado por pares

Functional Organization of Rat Olfactory Bulb Glomeruli Revealed by Optical Imaging

1998; Society for Neuroscience; Volume: 18; Issue: 7 Linguagem: Inglês

10.1523/jneurosci.18-07-02602.1998

ISSN

1529-2401

Autores

Asaf Keller, Sergey Yagodin, Vassiliki Aroniadou‐Anderjaska, Lee A. Zimmer, Matthew Ennis, N. Sheppard, Michael T. Shipley,

Tópico(s)

Advanced Chemical Sensor Technologies

Resumo

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 GABA A receptor antagonist bicuculline methiodide had little effect, whereas the GABA B receptor agonist baclofen dramatically attenuated ONL-evoked synaptic responses. The effects of baclofen were reversed by the GABA B 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 GABA A receptor-mediated inhibition has little effect on these responses, and that GABA B receptor-mediated inhibition may act presynaptically on olfactory nerve axons to modulate their inputs to olfactory bulb neurons.

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