Resting and reactive astrocytes express adrenergic receptors in the adult rat brain

Adrenergic receptor subtypes were localized in situ and in cells isolated from the trigeminal motor nucleus and several other brain regions. To study receptor expression in reactive astrocytes, motor neuron degeneration and a glial reaction were induced in the trigeminal motor nucleus by the injection of the toxic lectin Ricin communis into the trigeminal motor root. Autoradiography following incubation of tissue sections in the alpha 1-ligand 125IBE 2254 (HEAT) or the beta-ligand 125Iodocyanopindolol (ICYP) showed a decrease in alpha 1- and an increase in beta-adrenergic receptor binding in the region of neuronal degeneration and gliosis. Glial hypertrophy, rather than hyperplasia, appears to be mainly responsible for the increased beta-binding, since inhibition of mitosis with cytosine arabinofuranoside only partially blocked elevations of beta-adrenergic receptor binding and GFAP immunolabelling in reactive astrocytes. More direct evidence for the expression of adrenergic receptors in normal and reactive astrocytes was obtained by combined autoradiography and immunohistochemistry of cells dissociated from the cerebral cortex, striatum, cerebellum, and trigeminal motor nucleus of adult rats. More than 88% of GFAP-positive astrocytes showed varying densities of beta-adrenergic receptor binding. In each region, the beta 2-subtype was proportionally greater than the beta 1-subtype. Astrocytes also expressed a significant density of alpha 1-receptors. Trigeminal motor neurons did not show beta-receptor binding, but had a density of alpha 1-receptors tenfold greater than astrocytes. A model for the role of astrocytes in adrenergic receptor-mediated modulation of trigeminal motor neuron excitability is discussed.