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J Neurophysiol 85: 1275-1282, 2001;
0022-3077/01 $5.00
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The Journal of Neurophysiology Vol. 85 No. 3 March 2001, pp. 1275-1282
Copyright ©2001 by the American Physiological Society

Dendritic Glutamate Autoreceptors Modulate Signal Processing in Rat Mitral Cells

Paul-Antoine Salin,1,2,3 Pierre-Marie Lledo,3 Jean-Didier Vincent,3 and Serge Charpak1

 1Laboratory of Physiology, Ecole Supérieure de Physique et Chimie, 75005 Paris;  2Centres des Sciences du Goût-Centre National de la Recherche Scientifique, 21000 Dijon; and  3Centre National de la Recherche Scientifique, Institut Alfred Fessard, 91198 Gif sur Yvette, France

Salin, Paul-Antoine, Pierre-Marie Lledo, Jean-Didier Vincent, and Serge Charpak. Dendritic Glutamate Autoreceptors Modulate Signal Processing in Rat Mitral Cells. J. Neurophysiol. 85: 1275-1282, 2001. It has been shown recently that in mitral cells of the rat olfactory bulb, N-methyl-D-aspartate (NMDA) autoreceptors are activated during mitral cell firing. Here we consider in more details the mechanisms of mitral cell self-excitation and its physiological relevance. We show that both ionotropic NMDA and non-NMDA autoreceptors are activated by glutamate released from primary and secondary dendrites. In contrast to non-NMDA autoreceptors, NMDA autoreceptors are almost exclusively located on secondary dendrites and their activation generates a large and sustained self-excitation. Both intracellularly evoked and miniature NMDA-R mediated synaptic potentials are blocked by intracellular bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA) and result from a calcium-dependent release of glutamate. Self-excitation can be produced by a single spike, and trains of spikes result in frequency facilitation. Thus activation of excitatory autoreceptors is a major function of action potentials backpropagating in mitral cell dendrites, which results in an immediate positive feedback counteracting recurrent inhibition and increasing the signal-to-noise ratio of olfactory inputs.




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