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The Journal of Neurophysiology Vol. 86 No. 4 October 2001, pp. 1612-1621
Copyright ©2001 by the American Physiological Society
1Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5; and 2Center for Research in Neuroscience, Montreal General Hospital Research Institute, Montreal, Quebec H3G 1A4, H3A 1B1, Canada
Berman, Neil,
Robert J. Dunn, and
Leonard Maler.
Function of NMDA Receptors and Persistent Sodium Channels in
a Feedback Pathway of the Electrosensory System. J. Neurophysiol. 86: 1612-1621, 2001. Voltage-dependent
amplification of ionotropic glutamatergic excitatory postsynaptic
potentials (EPSPs) can, in many vertebrate neurons, be due either to
the intrinsic voltage dependence of N-methyl-D-aspartate (NMDA) receptors, or
voltage-dependent persistent sodium channels expressed on postsynaptic
dendrites or somata. In the electrosensory lateral line lobe (ELL) of
the gymnotiform fish Apteronotus leptorhynchus,
glutamatergic inputs onto pyramidal cell apical dendrites provide a
system where both amplification mechanisms are possible. We have now
examined the roles for both NMDA receptors and sodium channels in the
control of EPSP amplitude at these synapses. An antibody specific for
the A. leptorhynchus NR1 subunit reacted strongly with ELL
pyramidal cells and were particularly abundant in the spines of
pyramidal cell apical dendrites. We have also shown that NMDA receptors
contributed strongly to the late phase of EPSPs evoked by stimulation
of the feedback fibers terminating on the apical dendritic spines;
further, these EPSPs were voltage dependent. Blockade of NMDA receptors
did not, however, eliminate the voltage dependence of these EPSPs.
Blockade of somatic sodium channels by local somatic ejection of
tetrodotoxin (TTX), or inclusion of QX314 (an intracellular sodium
channel blocker) in the recording pipette, reduced the evoked EPSPs and completely eliminated their voltage dependence. We therefore conclude that, in the subthreshold range, persistent sodium currents are the
main contributor to voltage-dependent boosting of EPSPs, even when they
have a large NMDA receptor component.
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