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The Journal of Neurophysiology Vol. 83 No. 1 January 2000, pp. 315-321
Copyright ©2000 by the American Physiological Society
Department of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294
DeFazio, R. Anthony and
John J. Hablitz.
Alterations in NMDA Receptors in a Rat Model of Cortical
Dysplasia. J. Neurophysiol. 83: 315-321, 2000. Recent studies have demonstrated an important role for the
N-methyl-D-aspartate receptor (NMDAR) in
epilepsy. NMDARs have also been shown to play a critical role in
hyperexcitability associated with several animal models of human
epilepsy. Using whole-cell voltage clamp recordings in brain slices, we
studied evoked paroxysmal discharges in the freeze-lesion model of
neocortical microgyria. The voltage dependence of epileptiform
discharges indicated that these paroxysmal events were produced by a
complex pattern of excitatory and inhibitory inputs. We examined the
effect of the NMDAR antagonist D-2-amino-5-phosphopentanoic
acid (APV) and the NMDA receptor subunit type 2B
(NR2B)-selective antagonist ifenprodil on the threshold, peak
amplitude, and area of evoked epileptiform discharges in brain slices
from lesioned animals. Both compounds consistently raised the threshold
for evoking the discharge but had modest effects on the discharge peak
and amplitude. For comparison with nonlesioned cortex, we examined the
effects of ifenprodil on the epileptiform discharge evoked in the
presence of 2 µM bicuculline (partial disinhibition). In slices from
nonlesioned cortex, 10 µM ifenprodil had little effect on the
threshold whereas 71% of the recordings in bicuculline-treated
lesioned cortex showed a >25% increase in threshold. These results
suggest that NR2B-containing receptors are functionally enhanced in
freeze-lesioned cortex and may contribute to the abnormal
hyperexcitability observed in this model of neocortical microgyria.
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