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J Neurophysiol 98: 1052-1056, 2007. First published June 13, 2007; doi:10.1152/jn.01214.2006
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Endogenous GABA and Glutamate Finely Tune the Bursting of Olfactory Bulb External Tufted Cells

Abdallah Hayar1 and Matthew Ennis2

1Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas; and 2Department of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, Tennessee

Submitted 17 November 2006; accepted in final form 7 June 2007

In rat olfactory bulb slices, external tufted (ET) cells spontaneously generate spike bursts. Although ET cell bursting is intrinsically generated, its strength and precise timing may be regulated by synaptic input. We tested this hypothesis by analyzing whether the burst properties are modulated by activation of ionotropic {gamma}-aminobutyric acid (GABA) and glutamate receptors. Blocking GABAA receptors increased—whereas blocking ionotropic glutamate receptors decreased—the number of spikes/burst without changing the interburst frequency. The GABAA agonist (isoguvacine, 10 µM) completely inhibited bursting or reduced the number of spikes/burst, suggesting a shunting effect. These findings indicate that the properties of ET cell spontaneous bursting are differentially controlled by GABAergic and glutamatergic fast synaptic transmission. We suggest that ET cell excitatory and inhibitory inputs may be encoded as a change in the pattern of spike bursting in ET cells, which together with mitral/tufted cells constitute the output circuit of the olfactory bulb.

Address for reprint requests and other correspondence: A. Hayar, University of Arkansas for Medical Sciences, Dept. of Neurobiology and Developmental Sciences, 4301 West Markham Street Slot #847, Little Rock, AR 72205 (E-mail: abdallah{at}hayar.net)




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