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The Journal of Neurophysiology Vol. 82 No. 1 July 1999, pp. 489-494
Copyright ©1999 by the American Physiological Society
RAPID COMMUNICATION
Department of Anatomy and Neurobiology and Program in Neuroscience, University of Maryland School of Medicine, Baltimore, Maryland 21201
Aroniadou-Anderjaska, Vassiliki,
Matthew Ennis, and
Michael T. Shipley.
Dendrodendritic Recurrent Excitation in Mitral Cells of the Rat
Olfactory Bulb. J. Neurophysiol. 82: 489-494, 1999.
Most neuronal interactions within the olfactory
bulb network are mediated by dendrodendritic synapses. Dendritic
transmitter release potentially could affect the parent dendrite as
well as local neuronal elements that have receptors for the released
transmitter. Here we report that under conditions that facilitate
N-methyl-D-aspartate (NMDA) receptor activity
(reduced GABAA inhibition and extracellular Mg2+), a single action potential evoked by brief
intracellular current pulses in mitral cells is followed by a prolonged
depolarization, which is blocked by an NMDA receptor antagonist. This
depolarization also is evoked by a presumed calcium spike in the
presence of tetrodotoxin. A similar NMDA-receptor-dependent prolonged
depolarization is elicited by stimulation of the lateral olfactory
tract at current intensities subthreshold for antidromic activation of
the recorded neuron. These observations suggest that glutamate released
from the dendrites of mitral cells excites the same and neighboring mitral cell dendrites. Further evidence suggests that both the apical
and lateral dendrites of mitral cells participate in this recurrent
excitation. These dendrodendritic interactions may play a role in the
prolonged, NMDA-receptor-dependent depolarization of mitral/tufted
cells evoked by olfactory nerve stimulation.
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