TY - JOUR
T1 - Neocortical and hippocampal changes after multiple pilocarpine-induced status epilepticus in rats
AU - Da Silva, Alexandre Valotta
AU - Regondi, Maria Cristina
AU - Cipelletti, Barbara
AU - Frassoni, Carolina
AU - Abrão Cavalheiro, Esper
AU - Spreafico, Roberto
PY - 2005/5
Y1 - 2005/5
N2 - 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.
AB - 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.
KW - Early insult
KW - Immature brain
KW - Immunocytochemistry
KW - Immunohistoblot
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U2 - 10.1111/j.1528-1167.2005.31604.x
DO - 10.1111/j.1528-1167.2005.31604.x
M3 - Article
C2 - 15857427
AN - SCOPUS:18244393176
VL - 46
SP - 636
EP - 642
JO - Epilepsia
JF - Epilepsia
SN - 0013-9580
IS - 5
ER -