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Neocortical and Hippocampal Changes after Multiple Pilocarpine‐induced Status Epilepticus in Rats
Author(s) -
Valotta da Silva Alexandre,
Regondi Maria Cristina,
Cipelletti Barbara,
Frassoni Carolina,
Cavalheiro Esper Abrão,
Spreafico Roberto
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.1528-1167.2005.31604.x
Subject(s) - status epilepticus , pilocarpine , hippocampal formation , neuroscience , epilepsy , medicine , hippocampus , psychology
Summary: Purpose: Multiple episodes of pilocarpine‐induced status epilepticus (SE) in developing rats (P7–P9) lead to progressive epileptiform activity and severe cognitive impairment in adulthood. The present work studied possible underlying abnormalities in the neocortex and hippocampus of pilocarpine‐treated animals. Methods: Wistar rats were submitted to pilocarpine‐induced SE at P7, P8, and P9, and were killed at P35. Immunocytochemistry was performed on 50‐μm vibratome sections, by using antibodies against nonphosphorylated neurofilament (SMI‐311), parvalbumin (PV), calbindin (CB), calretinin (CR), and glutamate decarboxylase (GAD‐65). Ten‐micron cryostat sections were processed for immunohistoblot by using antibodies against GluR1, GluR2/3, and GluR4 α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA) receptor subunits and NR2ab N ‐methyl‐ d ‐aspartate (NMDA) receptor subunit. Results: Adult rats submitted to SE at P7–9 showed: (a) altered distribution of neocortical interneurons; (b) increased cortical and reduced hippocampal GAD‐65 expression; and (c) altered expression of hippocampal AMPA and NMDA receptors. Conclusions: We conclude that multiple SE episodes during P7–9 generate long‐lasting disturbances that underlie behavioral and electrographic abnormalities later in life.