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Journal of Neuroscience, Vol 15, 152-164, Copyright © 1995 by Society for Neuroscience
Beta 2-adrenergic receptors are expressed by glia in vivo in the normal and injured central nervous system in the rat, rabbit, and human
PW Mantyh, SD Rogers, CJ Allen, MD Catton, JR Ghilardi, LA Levin, JE Maggio and SR Vigna
Molecular Neurobiology Laboratory, Veterans Administration Medical Center, Minneapolis, Minnesota 55417.
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 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 alpha 1-, alpha 2-,
beta 1-, and beta 2-adrenergic receptors were identified in the rabbit and
rat forebrain. In the normal rabbit, rat, and human optic nerves, only
alpha 1 and beta 2 receptors were observed, and these were present in low
to moderate densities. Combined immunohistochemistry and autoradiography
suggests that the majority of beta 2-adrenergic receptors in the rabbit,
rat, and human optic nerve are expressed by astrocytes. After unilateral
optic nerve crush or transection, only beta 2- adrenergic receptors were
significantly increased. This increase in beta 2 receptors was first
detectable at days 7 and 28 post-transection in the rabbit and rat,
respectively. The expression of beta 2 receptors in the transected optic
nerve continued to increase with time, so that by 90 d post-transection the
density of beta 2 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, beta 2-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.
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