Abstract
BackgroundCBA/J mice are standard experimental animals in auditory studies, and age-related changes in auditory pathways are well documented. However, changes in locomotion-related brain regions have not been systematically explored.ResultsWe showed an increase in immunoreactivity for glial fibrillary acidic protein (GFAP) in the cerebellar molecular layer associated with Purkinje cells in mice at 24 weeks of age but not in the younger mice. Increased GFAP immunoreactivity appeared in the form of clusters and distributed multifocally consistent with hyperplasia of astrocytes that were occasionally associated with Purkinje cell degeneration. Three out of 12 animals at 16 and 24 weeks of age exhibited pre-convulsive clinical signs. Two of these 3 animals also showed increased GFAP immunoreactivity in the cerebellum. Rotarod behavioral assessments indicated decreased performance at 24 weeks of age.ConclusionsThese results suggest minimal to mild reactive astrocytosis likely associated with Purkinje cell degeneration in the cerebellum at 24 weeks of age in CBA/J mice. These findings should be taken into consideration prior to using this mouse strain for studying neuroinflammation or aging.
Highlights
CBA/J mice are standard experimental animals in auditory studies, and age-related changes in auditory pathways are well documented
Histopathologic examination of the striatum, corpus callosum and motor cortex There were no light microscopic findings in these structures in sections stained with hematoxylin and eosin (H&E, Figure S1) or glial fibrillary acidic protein (GFAP) immunochemistry (IHC, Figure S2) in any animals
Histopathologic examination of the cerebellum and medulla oblongata There were no histopathologic findings in Hematoxylin and eosin (H&E)-stained sections
Summary
CBA/J mice are standard experimental animals in auditory studies, and age-related changes in auditory pathways are well documented. The CBA/J mouse has become a standard experimental animal in auditory and hearing loss studies [1,2,3,4]. This strain has been crossed with C57BL/6 mice to generate a Huntington’s disease model [5, 6]. Tyszkiewicz et al Laboratory Animal Research (2021) 37:24 pathways in the brain have been well documented across the lifespan of this strain, locomotion-related brain areas have not been systematically evaluated. We have examined gray and white matter as well as glial cells in two brain sections: (1) at the level of the striatum/corpus callosum and motor cortex and (2) at the level of cerebellum/medulla oblongata of CBA/J mice at 8 to 24 weeks of age using combined histologic, immunohistochemistry (ICH) and behavioral assessments
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