BETA(2)-ADRENERGIC RECEPTORS ARE EXPRESSED BY GLIA IN-VIVO IN THE NORMAL AND INJURED CENTRAL-NERVOUS-SYSTEM IN THE RAT, RABBIT, AND HUMAN

Previous studies have demonstrated that glial cells in culture express several subtypes of functional adrenergic receptors. To determine if similar receptors are expressed by glia in vivo, we examined the expre ssion of adrenergic receptors in the normal, crushed, and transected o ptic nerves of the rabbit and rat using quantitative receptor autoradi ography. Additionally, we examined the expression of adrenergic recept ors in the normal and damaged human optic nerve. High levels of alpha( 1)-, alpha(2)-, beta(1)-, and beta(2)-adrenergic receptors were identi fied in the rabbit and rat forebrain. In the normal rabbit, rat, and h uman optic nerves, only alpha(1) beta(2) receptors were observed, and these were present in low to moderate densities. Combined immunohistoc hemistry and autoradiography suggests that the majority of beta(2)-adr energic receptors in the rabbit, rat, and human optic nerve are expres sed by astrocytes. After unilateral optic nerve crush or transection, only beta(2) adrenergic receptors were significantly increased. This i ncrease in beta(2) receptors was first detectable at days 7 and 28 pos t-transection in the rabbit and rat, respectively. The expression of b eta(2) receptors in the transected optic nerve continued to increase w ith time, so that by 90 d post-transection the density of beta(2) rece ptors in both the rabbit and rat optic nerve was among the highest of any area in the forebrain. Taken together with previous studies, these results suggest that in vivo, beta(2)-adrenergic receptors may provid e a therapeutic target for regulation of astrocyte functions including glycogen metabolism, cytokine release, and the hypertrophy and prolif eration that occurs in response to neuronal injury.