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The Journal of Neurophysiology Vol. 81 No. 2 February 1999, pp. 564-574
Copyright ©1999 by the American Physiological Society
1Departments of Neurology and 2Anatomy, and 3The Neuroscience Training Program, University of Wisconsin, and the 4William S. Middleton Veterans Administration Hospital, Madison, WI 53792
NMDA-dependent currents in granule cells of the dentate gyrus
contribute to induction but not permanence of kindling.
Single-electrode voltage-clamp techniques and bath application of the
N-methyl-D-aspartate (NMDA) receptor antagonist
2-amino-5-phosphonovaleric acid (APV) were used to study the time
course of seizure-induced alterations in NMDA-dependent synaptic
currents in granule cells of the dentate gyrus in hippocampal slices
from kindled and normal rats. In agreement with previous studies,
granule cells from kindled rats examined within 1 wk after the last of
3 or 30-35 generalized tonic-clonic (class V) seizures demonstrated an
increase in the NMDA receptor-dependent component of the perforant
path-evoked synaptic current. Within 1 wk of the last kindled seizure,
NMDA-dependent charge transfer underlying the perforant path-evoked
current was increased by 63-111% at a holding potential of 
30 mV.
In contrast, the NMDA-dependent component of the perforant-evoked
current in granule cells examined at 2.5-3 mo after the last of 3 or
90-120 class V seizures did not differ from age-matched controls.
Because the seizure-induced increases in NMDA-dependent synaptic
currents declined toward control values during a time course of 2.5-3
mo, increases in NMDA-dependent synaptic transmission cannot account
for the permanent susceptibility to evoked and spontaneous seizures
induced by kindling. The increase in NMDA receptor-dependent
transmission was associated with the induction of kindling but was not
responsible for the maintenance of the kindled state. The time course
of alterations in NMDA-dependent synaptic current and the dependence of
the progression of kindling and kindling-induced mossy fiber sprouting
on repeated NMDA receptor activation are consistent with the
possibility that the NMDA receptor is part of a transmembrane signaling
pathway that induces long-term cellular alterations and circuit
remodeling in response to repeated seizures, but is not required for
permanent seizure susceptibility in circuitry altered by
kindling.
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