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

Abstract

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 α 1-ligand 125IBE 2254 (HEAT) or the β-ligand 125Iodocyanopindolol (ICYP) showed a decrease in α 1- and an increase in β-adrenergic receptor binding in the region of neuronal degeneration and gliosis. Glial hypertrophy, rather than hyperplasia, appears to be mainly responsible for the increased β-binding, since inhibition of mitosis with cytosine arabinofuranoside only partially blocked elevations of β-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 β-adrenergic receptor binding. In each region, the β 2-subtype was proportionally greater than the β 1-subtype. Astrocytes also expressed a significant density of α 1-receptors. Trigeminal motor neurons did not show β-receptor binding, but had a density of α 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.