title: Glial alterations in the hippocampus of rats submitted to ibotenic-induced lesion of the nucleus basalis magnocellularis.
abstract: Lesion of the nucleus basalis magnocellularis (nbm) is a suitable approach to study cognitive deficit and behavior alterations involving cholinergic dysfunction, which is associated with the major types of dementia. Cortical astrogliosis also has been described in this model, but it is not clear whether hippocampal astrocytes are activated. In this study, we investigated possible specific astrocyte alterations in the hippocampi of Wistar rats submitted to nbm damage with ibotenic acid, investigating the content and immunohistochemistry of glial fibrillary acidic protein (GFAP), as well as S100B protein content, glutamate uptake and glutamine synthetase activity on the 7th and 28th post-lesion days. Cognitive deficit was confirmed by the step-down inhibitory avoidance task. Interestingly, we found a decrease in GFAP content, S100B content and glutamate uptake activity in the hippocampus on the 28th day after nbm lesion. No alterations were observed in glutamine synthetase activity or in the cerebrospinal fluid S100B content. Although our data suggest caution in the use of nbm lesion with ibotenic acid as a dementia model, it is possible that these alterations could contribute to the cognitive deficit observed in these rats.
authors.affiliation: Programa de Pós-Graduação em Neurociências, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Sarmento Leite, 500, 90050-170, Porto Alegre, RS, Brazil.
authors.forename: Alessandra
authors.initials: A
authors.lastname: Swarowsky
authors.forename: Letícia
authors.initials: L
authors.lastname: Rodrigues
authors.forename: Regina
authors.initials: R
authors.lastname: Biasibetti
authors.forename: Marina C
authors.initials: MC
authors.lastname: Leite
authors.forename: Lucas Fürstenau
authors.initials: LF
authors.lastname: de Oliveira
authors.forename: Lucia M V
authors.initials: LM
authors.lastname: de Almeida
authors.forename: Carmem
authors.initials: C
authors.lastname: Gottfried
authors.forename: Jorge A
authors.initials: JA
authors.lastname: Quillfeldt
authors.forename: Matilde
authors.initials: M
authors.lastname: Achaval
authors.forename: Carlos-Alberto
authors.initials: CA
authors.lastname: Gonçalves
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000166:cytology* / Q000378:metabolism; D001362:Avoidance Learning / Q000502:physiology*; D020532:Basal Nucleus of Meynert / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D001925:Brain Damage, Chronic / Q000139:chemically induced; D002452:Cell Count; D002799:Cholinergic Fibers / Q000378:metabolism*; D003704:Dementia / Q000378:metabolism / Q000503:physiopathology*; D004195:Disease Models, Animal; D005106:Exploratory Behavior / Q000502:physiology; D005500:Follow-Up Studies; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005974:Glutamate-Ammonia Ligase / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D006185:Habituation, Psychophysiologic / Q000502:physiology; D006624:Hippocampus / Q000166:cytology* / Q000378:metabolism; D007051:Ibotenic Acid; D007150:Immunohistochemistry; D008297:Male; D009414:Nerve Growth Factors / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000378:metabolism; D018709:Statistics, Nonparametric; D013997:Time Factors
chemical_list: D005904:Glial Fibrillary Acidic Protein; D009414:Nerve Growth Factors; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; C579158:S100b protein, rat; D007051:Ibotenic Acid; D018698:Glutamic Acid; D005974:Glutamate-Ammonia Ligase