Astrocytes express several cell surface receptors including the β2- adrenergic receptor. To explore whether β-adrenergic receptors (β-ARs) directly regulate astrogliosis and glial scar formation, we evaluated the effects of β-AR activation and blockade on astrocyte hypertrophy and cell proliferation in rabbit optic nerves in vivo. Artificial cerebrospinal fluid (CSF), isoproterenol (ISO; a β-agonist), or propranolol (PROP; a β- antagonist) were infused via osmotic minipumps into non-injured and crushed optic nerves for 14 days. Changes in nerve cell numbers and astroglial hypertrophy were monitored by ethidium bromide nuclear staining and glial fibrillary acidic protein (GFAP) immunohistochemistry, respectively. In non- injured nerves infused with CSF or PROP, there were no alterations in GFAP- immunoreactivity or cell numbers compared to normal optic nerves; however, in non-injured nerves infused with ISO, there was a significant increase in both GFAP-immunoreactivity and cell number. In crushed optic nerves, there was a significant increase in both GFAP-immunoreactivity and cell number compared to normal nerves, and this increase was not altered by infusion of either CSF or ISO. In contrast, PROP infusion significantly reduced the crush-induced increase in GFAP-immunofluorescence and cell number. These findings suggest that a) β-AR activation, in the absence of injury, can promote astroglial hypertrophy and cell proliferation; b) after injury, β- AR activation drives injury-induced astrogliosis and cell proliferation; c) astrocyte β-ARs are maximally stimulated after neuronal injury; and d) neuronal regeneration may be influenced, both positively and negatively, through the pharmacological manipulation of glial receptors.
|Original language||English (US)|
|Number of pages||11|
|State||Published - May 1996|
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience