Journal
NEUROREPORT
Volume 27, Issue 16, Pages 1191-1195Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/WNR.0000000000000656
Keywords
GluN2B; long-term potentiation; status epilepticus; synapse
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Funding
- Russian Science Foundation [16-15-10202]
- Russian Science Foundation [16-15-10202] Funding Source: Russian Science Foundation
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Seizure-induced memory deficits are frequent in patients with temporal lobe epilepsy. However, the neural mechanisms responsible for this memory impairment are not entirely clear. Persistent changes in synaptic efficacy, long-term potentiation (LTP), and depression are considered a cellular substrate underlying the learning and memory processes. Using a lithium-pilocarpine model to induce status epilepticus (SE) in rats, the present study investigated whether the induction of LTP was altered in hippocampal slices obtained 3h, 1, 3, and 7 days after SE. One week after SE, LTP induction was decreased in hippocampal slices. The reduced plasticity in post-SE tissue was attributable to N-methyl-d-aspartate receptor-dependent LTP. In contrast to control tissue, ifenprodil, a GluN2B-selective antagonist, did not reduce the LTP level in post-SE tissue, suggesting that SE disturbs the functional properties of GluN2B-containing N-methyl-d-aspartate receptors. These changes in synaptic transmission may contribute toward the genesis of epilepsy and seizure-associated memory deficits.
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