Open AccessEarly‐Life Seizures and Cognitive Impairment: A Spiny Problem?
Author(s) -
Stafstrom Carl E.,
Benke Timothy A.
Publication year - 2007
Publication title -
epilepsy currents
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.415
H-Index - 22
eISSN - 1535-7511
pISSN - 1535-7597
DOI - 10.1111/j.1535-7511.2007.00225.x
Subject(s) - glutamatergic , neocortex , neuroscience , nmda receptor , hippocampus , hippocampal formation , epilepsy , epileptogenesis , dendritic spine , synapse , glutamate receptor , kindling , medicine , receptor , psychology
Swann JW, Le JT, Lee CL. Dev Neurosci 2007;29(1–2):168–178. Recurrent seizures in animal models of early‐onset epilepsy have been shown to produce deficits in spatial learning and memory. While neuronal loss does not appear to underlie these effects, dendritic spine loss has been shown to occur. In experiments reported here, seizures induced either by tetanus toxin or flurothyl during the second postnatal week were found to reduce the expression of NMDA receptor subunits in both the hippocampus and neocortex. Most experiments focused on alterations in the expression of the NR2A subunit and its associated scaffolding protein, PSD95, since their expression is developmentally regulated. Results suggest that the depression in expression can be delayed by at least 5 days but persists for at least 3‐4 weeks. These effects were dependent on the number of seizures experienced, and were not observed when seizures were induced in adult mice. Taken together, the results suggest that recurrent seizures in infancy may interrupt synapse maturation and produce persistent decreases in molecular markers for glutamatergic synapses – particularly components of the NMDA receptor complex implicated in learning and memory.