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The Journal of Neurophysiology Vol. 84 No. 4 October 2000, pp. 1881-1887
Copyright ©2000 by the American Physiological Society
ková,1,2,4 and1Department of Neurology, 2Department of Neuroscience, and 3Department of Pediatrics, Albert Einstein College of Medicine; and 4Center for Epilepsy Management, Montefiore Medical Center, Bronx 10461; 5Mercy College, Dobbs Ferry, New York 10522; and 6Novartis Pharmaceuticals, East Hanover, New Jersey 06851
Hedberg, Thomas G.,
Ellen F. Sperber,
Jana Velí
ková, and
Solomon L. Moshé.
Laminar and Temporal Heterogeneity of NMDA/Metabotropic Glutamate
Receptor Binding in Posterior Cingulate Cortex. J. Neurophysiol. 84: 1881-1887, 2000. Both
N-methyl-D-aspartate (NMDA) and
quisqualate/AMPA-insensitive metabotropic glutamate (mGlu) receptors
mediate plasticity induction in neocortex, but their interlaminar
distribution in cortical microcircuits is largely unknown. We used
(+)3H-MK801 and
3H-glutamate binding plus saturating
concentrations of NMDA, AMPA, and quisqualate to autoradiographically
map NMDA and mGlu receptor sites by lamina in posterior cingulate
cortex in adult male rats. Specific binding at NMDA receptor sites in
laminae II/III and VI was significantly reduced in comparison to other
laminae. Brains prepared from rats killed during dark phase of a
12h/12h light/dark cycle showed a mean 129% increase in overall
(+)3H-MK801 binding versus light phase brains but
retained reduced binding densities in laminae II/III and VI. In
contrast to NMDA findings, specific binding at mGlu sites was
consistently elevated during light phase in both laminae II/III and VI.
Specific 3H-glutamate binding in dark-phase
brains showed an overall 147% increase versus light phase binding but
did not retain significant interlaminar heterogeneity. Interpreted in
accordance with our physiologically derived models of
hippocampo-cortical microcircuitry, these results suggest that spatial
and temporal variations in glutamate receptor distribution may play an
important role in intracingulate neural processing of afferent input
from hippocampus.
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