β2 -adrenergic receptors are expressed by glia in vivo in the normal and injured central nervous system in the rat, rabbit, and human

Journal Article

Previous studies have demonstrated that glial cells in culture express several subtypes of functional adrenergic receptors. To determine if similar receptors are expressed by gila in vivo, we examined the expression of adrenergic receptors in the normal, crushed, and transected optic nerves of the rabbit and rat using quantitative receptor autoradiography. Additionally, we examined the expression of adrenergic receptors in the normal and damaged human optic nerve. High levels of α1-, α2-, β1-, and β2-adrenergic receptors were identified in the rabbit and rat forebrain. In the normal rabbit, rat, and human optic nerves, only α1 and β2 receptors were observed, and these were present in low to moderate densities. Combined immunohistochemistry and autoradiography suggests that the majority of β2- adrenergic receptors in the rabbit, rat, and human optic nerve are expressed by astrocytes. After unilateral optic nerve crush or transection, only β2- adrenergic receptors were significantly increased. This increase in β2 receptors was first detectable at days 7 and 28 post-transection in the rabbit and rat, respectively. The expression of β2 receptors in the transected optic nerve continued to increase with time, so that by 90 d post- transection the density of β2 receptors 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, β2-adrenergic receptors may provide a therapeutic target for regulation of astrocyte functions including glycogen metabolism, cytokine release, and the hypertrophy and proliferation that occurs in response to neuronal injury.

Duke Authors

Cited Authors

  • Mantyh, PW; Rogers, SD; Allen, CJ; Catton, MD; Ghilardi, JR; Levin, LA; Maggio, JE; Vigna, SR

Published Date

  • 1995

Published In

  • Journal of Neuroscience

Volume / Issue

  • 15 / 1 I

Start / End Page

  • 152 - 164