title: Astroglial loss and edema formation in the rat piriform cortex and hippocampus following pilocarpine-induced status epilepticus.
abstract: In the present study we analyzed aquaporin-4 (AQP4) immunoreactivity in the piriform cortex (PC) and the hippocampus of pilocarpine-induced rat epilepsy model to elucidate the roles of AQP4 in brain edema following status epilepticus (SE). In non-SE-induced animals, AQP4 immunoreactivity was diffusely detected in the PC and the hippocampus. AQP4 immunoreactivity was mainly observed in the endfeet of astrocytes. Following SE the AQP4-deleted area was clearly detected in the PC, not in the hippocampus. Decreases in dystrophin and α-syntrophin immunoreactivities were followed by reduction in AQP4 immunoreactivity. These alterations were accompanied by the development of vasogenic edema and the astroglial loss in the PC. In addition, acetazolamide (an AQP4 inhibitor) treatment exacerbated vasogenic edema and astroglial loss both in the PC and in the hippocampus. These findings suggest that SE may induce impairments of astroglial AQP4 functions via disruption of the dystrophin/α-syntrophin complex that worsen vasogenic edema. Subsequently, vasogenic edema results in extensive astroglial loss that may aggravate vasogenic edema.
authors.affiliation: Department of Anatomy and Neurobiology, College of Medicine, Hallym University, Chunchon, Kangwon-Do 200-702, South Korea.
authors.forename: Ji-Eun
authors.initials: JE
authors.lastname: Kim
authors.forename: Seong-Il
authors.initials: SI
authors.lastname: Yeo
authors.forename: Hea Jin
authors.initials: HJ
authors.lastname: Ryu
authors.forename: Min-Ju
authors.initials: MJ
authors.lastname: Kim
authors.forename: Duk-Soo
authors.initials: DS
authors.lastname: Kim
authors.forename: Seung-Mook
authors.initials: SM
authors.lastname: Jo
authors.forename: Tae-Cheon
authors.initials: TC
authors.lastname: Kang
mesh_terms: D000818:Animals; D051401:Aquaporin 4 / Q000378:metabolism; D001253:Astrocytes / Q000473:pathology*; D001929:Brain Edema / Q000209:etiology*; D002135:Calcium-Binding Proteins / Q000378:metabolism; D002452:Cell Count / Q000379:methods; D002540:Cerebral Cortex / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D016189:Dystrophin / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006624:Hippocampus / Q000473:pathology / Q000503:physiopathology*; D018021:Lithium Chloride / Q000633:toxicity; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D009124:Muscle Proteins / Q000378:metabolism; D010862:Pilocarpine / Q000633:toxicity; D051381:Rats; D017207:Rats, Sprague-Dawley; D013226:Status Epilepticus / Q000139:chemically induced / Q000150:complications* / Q000473:pathology*
chemical_list: C496032:Aqp4 protein, rat; D051401:Aquaporin 4; D002135:Calcium-Binding Proteins; D016189:Dystrophin; D005904:Glial Fibrillary Acidic Protein; D008565:Membrane Proteins; D009124:Muscle Proteins; C091825:syntrophin alpha1; D010862:Pilocarpine; D018021:Lithium Chloride