Age‐induced hypertrophy of astrocytes in rat supraoptic nucleus: A cytological, morphometric, and immunocytochemical study

Publisher Website
Google Scholar
Abstract
Background: In the adult rat, neuron-astroglia interactions in the supraoptic nucleus (SON) are characterized by the structural and functional plasticity of astrocytes in response to several physiological and experimental conditions. This study has analyzed the plasticity of the supraoptic nucleus astrocytes in response to the age-induced changes in neuronal activity. Methods: The study was performed in 5-, 12-, 18- and 24-month-old rats. The cytology and organization of astrocytes in the SON were examined using glial fibrillary acidic and vimentin immunocytochemistry and ultrastructural and morphometric analysis. Results: No significant age-related variations in the total number of neurons and astrocytes in the SON were detected, although a few degenerating neurons were found in old rats. An age-dependent increase in GFAP immunoreactivity was observed at the ventral glial lamina, perivascularly and between neuronal perikarya. Vimentin overexpression was also detected in ventral lamina astrocytes with advancing age. At the cell nucleus level, we observed an age-associated increase in nuclear size and in the number of coiled bodies, nuclear bodies, and “cleared” nucleoplasmic areas, as well as changes in the nucleolar organization. At the cytoplasmic level, characteristic ultrastructural features in astrocytes of old rats were the hypertrophy of intermediate filament bundles and the formation of an extensive network of Golgi stacks interlinked by tubulovesicular elements. Glial filaments were often associated with the nuclear envelope and polyribosomes. Conclusions: The increased GFAP and vimentin immunoreactivity and the morphometric and cytological changes in rat SON astrocytes may reflect a sustained upregulation of cellular activity with age, resulting in hypertrophy of glial perikarya and cell processes. Several factors that are known to influence the expression of the astrocytic phenotype, such as signals produced by degenerating neurons and activated microglia, as well as variations in neuronal activity are considered possible causes of the age-associated changes in SON astrocytes.