Glial alterations in the hippocampus of rats submitted to ibotenic-induced lesion of the nucleus basalis magnocellularis

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 whe...

Full description

Saved in:
Bibliographic Details
Published inBehavioural brain research Vol. 190; no. 2; pp. 206 - 211
Main Authors Swarowsky, Alessandra, Rodrigues, Letícia, Biasibetti, Regina, Leite, Marina C., de Oliveira, Lucas Fürstenau, de Almeida, Lucia M.V., Gottfried, Carmem, Quillfeldt, Jorge A., Achaval, Matilde, Gonçalves, Carlos-Alberto
Format Journal Article
LanguageEnglish
Published Shannon Elsevier B.V 19.07.2008
Elsevier Science
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary: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.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ISSN:0166-4328
1872-7549
DOI:10.1016/j.bbr.2008.02.039