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1 Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
2 Department of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, Tennessee, United States
* To whom correspondence should be addressed. E-mail: abdallah{at}hayar.net.
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 GABA and glutamate receptors. Blocking GABAA receptors increased, whereas blocking ionotropic glutamate receptors decreased, the number of spikes/burst without changing the inter-burst 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.
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N. Karpuk and A. Hayar Activation of Postsynaptic GABAB Receptors Modulates the Bursting Pattern and Synaptic Activity of Olfactory Bulb Juxtaglomerular Neurons J Neurophysiol, January 1, 2008; 99(1): 308 - 319. [Abstract] [Full Text] [PDF] |
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