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J Neurophysiol 82: 1082-1085, 1999;
0022-3077/99 $5.00
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The Journal of Neurophysiology Vol. 82 No. 2 August 1999, pp. 1082-1085
Copyright ©1999 by the American Physiological Society

RAPID COMMUNICATION

Dopamine Depresses Synaptic Inputs Into the Olfactory Bulb

Albert Y. Hsia, Jean-Didier Vincent, and Pierre-Marie Lledo

Centre National de la Recherche Scientifique, Institut Alfred Fessard, 91198 Gif-sur-Yvette, France

Hsia, Albert Y., Jean-Didier Vincent, and Pierre-Marie Lledo. Dopamine Depresses Synaptic Inputs Into the Olfactory Bulb. J. Neurophysiol. 82: 1082-1085, 1999. Both observations in humans with disorders of dopaminergic transmission and molecular studies point to an important role for dopamine in olfaction. In this study we found that dopamine receptor activation in the olfactory bulb causes a significant depression of synaptic transmission at the first relay between olfactory receptor neurons and mitral cells. This depression was found to be caused by activation of the D2 subtype of dopamine receptor and was reversible by a specific D2 receptor antagonist. A change in paired-pulse modulation during the depression suggests a presynaptic locus of action. The depression was found to occur independent of synaptic activity. These results provide the first evidence for dopaminergic control of inputs to the main olfactory bulb. The magnitude and locus of dopamine's modulatory capabilities in the bulb suggest important roles for dopamine in odorant processing.




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