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J Neurophysiol 86: 2986-2997, 2001;
0022-3077/01 $5.00
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The Journal of Neurophysiology Vol. 86 No. 6 December 2001, pp. 2986-2997
Copyright ©2001 by the American Physiological Society

Dopamine D2 Receptor-Mediated Presynaptic Inhibition of Olfactory Nerve Terminals

Matthew Ennis,1 Fu-Ming Zhou,1 Kelly J. Ciombor,1 Vassiliki Aroniadou-Anderjaska,1 Abdallah Hayar,1 Emiliana Borrelli,2 Lee A. Zimmer,1 Frank Margolis,1 and Michael T. Shipley1

 1Department of Anatomy and Neurobiology and Program in Neuroscience, University of Maryland School of Medicine, Baltimore, Maryland 21201; and  2Institut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique/Institut National de la Santé et de la Recherche Médicale/Université Louis Pasteur, BP163, 67404 Illkirch Cedex, Strasbourg, France

Ennis, Matthew, Fu-Ming Zhou, Kelly J. Ciombor, Vassiliki Aroniadou-Anderjaska, Abdallah Hayar, Emiliana Borrelli, Lee A. Zimmer, Frank Margolis, and Michael T. Shipley. Dopamine D2 Receptor-Mediated Presynaptic Inhibition of Olfactory Nerve Terminals. J. Neurophysiol. 86: 2986-2997, 2001. Olfactory receptor neurons of the nasal epithelium project via the olfactory nerve (ON) to the glomeruli of the main olfactory bulb, where they form glutamatergic synapses with the apical dendrites of mitral and tufted cells, the output cells of the olfactory bulb, and with juxtaglomerular interneurons. The glomerular layer contains one of the largest population of dopamine (DA) neurons in the brain, and DA in the olfactory bulb is found exclusively in juxtaglomerular neurons. D2 receptors, the predominant DA receptor subtype in the olfactory bulb, are found in the ON and glomerular layers, and are present on ON terminals. In the present study, field potential and single-unit recordings, as well as whole cell patch-clamp techniques, were used to investigate the role of DA and D2 receptors in glomerular synaptic processing in rat and mouse olfactory bulb slices. DA and D2 receptor agonists reduced ON-evoked synaptic responses in mitral/tufted and juxtaglomerular cells. Spontaneous and ON-evoked spiking of mitral cells was also reduced by DA and D2 agonists, and enhanced by D2 antagonists. DA did not produce measurable postsynaptic changes in juxtaglomerular cells, nor did it alter their responses to mitral/tufted cell inputs. DA also reduced 1) paired-pulse depression of ON-evoked synaptic responses in mitral/tufted and juxtaglomerular cells and 2) the amplitude and frequency of spontaneous, but not miniature, excitatory postsynaptic currents in juxtaglomerular cells. Taken together, these findings are consistent with the hypothesis that activation of D2 receptors presynaptically inhibits ON terminals. DA and D2 agonists had no effect in D2 receptor knockout mice, suggesting that D2 receptors are the only type of DA receptors that affect signal transmission from the ON to the rodent olfactory bulb.




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