title: Short-term effects of kainic acid on CA1 hippocampal interneurons differentially vulnerable to excitotoxicity.
abstract: OBJECTIVE
  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 Ca2+ 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.
authors.affiliation: Centre de Recherche en Sciences Neurologiques, Département de Physiologie, Centre de recherche de l'Hôpital Sainte-Justine, Université de Montréal, Quebec, Canada.
authors.forename: Nathalie
authors.initials: N
authors.lastname: Sanon
authors.forename: Lionel
authors.initials: L
authors.lastname: Carmant
authors.forename: Martine
authors.initials: M
authors.lastname: Emond
authors.forename: Patrice
authors.initials: P
authors.lastname: Congar
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Lacaille
mesh_terms: D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000502:physiology; D004195:Disease Models, Animal; D004833:Epilepsy, Temporal Lobe / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology*; D005968:Glutamate Decarboxylase / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D007395:Interneurons / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D007608:Kainic Acid / Q000494:pharmacology*; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D010320:Parvalbumins / Q000378:metabolism; D018408:Patch-Clamp Techniques; D051381:Rats; D017207:Rats, Sprague-Dawley; D018091:Receptors, AMPA / Q000187:drug effects / Q000502:physiology; D017470:Receptors, Glutamate / Q000187:drug effects; D013004:Somatostatin / Q000378:metabolism; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D018690:Excitatory Amino Acid Agonists; D010320:Parvalbumins; D018091:Receptors, AMPA; D017470:Receptors, Glutamate; D013779:Tetrodotoxin; D013004:Somatostatin; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D005968:Glutamate Decarboxylase; D007608:Kainic Acid; D002118:Calcium