Status epilepticus alters hippocampal long-term synaptic potentiation in a rat lithium-pilocarpine model

• Published in: Neuroreport Vol. 27; no. 16; p. 1191
• Main Authors: Kryukov, Kirill A, Kim, Kira K, Magazanik, Lev G, Zaitsev, Aleksey V
• Format: Journal Article
• Language: English
• Published: England 09.11.2016
• Subjects: 2-Amino-5-phosphonovalerate - therapeutic use; Animals; Anticonvulsants - therapeutic use; Convulsants - toxicity; Disease Models, Animal; Hippocampus - drug effects; In Vitro Techniques; Lithium - toxicity; Long-Term Potentiation - drug effects; Patch-Clamp Techniques; Pilocarpine - toxicity; Rats; Rats, Wistar; Status Epilepticus - chemically induced; Status Epilepticus - pathology; Status Epilepticus - prevention & control; Time Factors
• ISSN: 1473-558X
• DOI: 10.1097/WNR.0000000000000656

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 3 h, 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.