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Short‐term Effects of Kainic Acid on CA1 Hippocampal Interneurons Differentially Vulnerable to Excitotoxicity
Author(s) -
Sa Nathalie,
Carmant Lionel,
Emond Martine,
Congar Patrice,
Lacaille JeanClaude
Publication year - 2005
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2005.21404.x
Subject(s) - kainic acid , excitotoxicity , neuroscience , hippocampal formation , term (time) , biology , medicine , glutamate receptor , physics , receptor , quantum mechanics
Summary: Purpose: We sought to identify the inhibitory interneurons of the rat hippocampal CA1 region selectively vulnerable in the kainic acid (KA) model of temporal lobe epilepsy and to determine whether their selective vulnerability could be due to differential short‐term KA effects. Methods : We quantified vulnerable interneurons in stratum oriens‐alveus (O/A) by using immunohistochemistry for glutamic acid decarboxylase (GAD), parvalbumin (PV), and somatostatin (SS) after KA injections in rats, and then compared in normal slices the effects of KA on interneurons either in O/A (vulnerable to KA) or in strata radiatum and lacunosum‐moleculare (R/LM) (resistant to KA) by using whole‐cell recording and calcium imaging. Results : GAD‐, PV‐ and SS‐positive cells in O/A were decreased after KA treatment in P20 and P30 rats. Both short (1‐min) and long (10‐min) applications of KA produced similar tetrodotoxin (TTX)‐insensitive membrane depolarization and decrease in input resistance in O/A and R/LM interneurons. KA responses were antagonized by CNQX and GYKI52466, suggesting AMPA receptor activation. KA also generated a similar increase in intracellular Ca 2+ in O/A and R/LM interneurons, which was antagonized by CNQX and GYKI52466. Conclusions : The selective vulnerability of GAD‐, PV‐, and SS‐immunopositive O/A interneurons in the KA model may not arise from cell‐specific short‐term membrane effects or calcium responses induced by KA, but from other glutamate receptor‐mediated excitotoxic processes.