Neuronal degeneration and gliosis time-course in the mouse hippocampal formation after pilocarpine-induced status epilepticus.
Temporal lobe epilepsy (TLE) is the most common type of human epilepsy and has been related with extensive loss of hippocampal pyramidal and dentate hilar neurons and gliosis. Many characteristics of TLE are reproduced in the pilocarpine model of epilepsy in mice. This study analyzed the neuronal damage, assessed with Fluoro-Jade (FJB) and cresyl violet, and gliosis, investigated with glial fibrilary acidic protein (GFAP) immunohistochemistry, occurring in the hippocampal formation of mice at 3, 6, 12 and 24h, 1 and 3 weeks after the pilocarpine-induced status-epilepticus (SE) onset. The maximum neuronal damage score and the FJB-positive neurons peak were found in the hilus of dentate gyrus 3 and 12 h after SE onset (P<0.05), respectively. At 1 week after SE onset, the greatest neuronal damage score was detected in the CA1 pyramidal cell layer and the greatest numbers of FJB-positive neurons were found both in the CA1 and CA3 pyramidal cell layers (P<0.05). The molecular, CA3 and CA1 pyramidal cell layers expressed highest presence of GFAP immunoreaction at 1 and 3 weeks after SE onset (P<0.05). Our findings show that, depending on the affected area, neuronal death and gliosis can occur within few hours or weeks after SE onset. Our results corroborate previous studies and characterize short time points of temporal evolution of neuropathological changes after the onset of pilocarpine-induced SE in mice and evidences that additional studies of this temporal evolution may be useful to the comprehension of the cellular mechanisms underlying epileptogenesis.
Department of Cell Biology, Biological Sciences Institute, University of Brasília-UnB, Brasília, DF, Brazil. andreluiz.nexp@gmail.com
André Luiz
AL
do Nascimento
Neide Ferreira
NF
Dos Santos
Fernanda
F
Campos Pelágio
Simone
S
Aparecida Teixeira
Elenice A
EA
de Moraes Ferrari
Francesco
F
Langone
D000704:Analysis of Variance; D000818:Animals; D016923:Cell Death / Q000187:drug effects; D004195:Disease Models, Animal; D018450:Disease Progression; D005452:Fluoresceins; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000209:etiology*; D006624:Hippocampus / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D051379:Mice; D009069:Movement Disorders / Q000209:etiology; D018721:Muscarinic Agonists / Q000633:toxicity; D009410:Nerve Degeneration / Q000209:etiology*; D009930:Organic Chemicals; D010862:Pilocarpine / Q000633:toxicity; D017966:Pyramidal Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D013226:Status Epilepticus / Q000139:chemically induced / Q000473:pathology*; D013997:Time Factors
D005452:Fluoresceins; D005904:Glial Fibrillary Acidic Protein; D018721:Muscarinic Agonists; D009930:Organic Chemicals; C435731:fluoro jade; D010862:Pilocarpine