Expression of adrenergic receptors in individual astrocytes and motor neurons isolated from the adult rat brain.
Attempts to show the distribution of adrenergic receptors (ARs) in autoradiographs of a brainstem motor nucleus following elimination of motor neurons yielded the unexpected result of an increase in beta-AR density. This increase was related to the gliosis accompanying the motor neuron degeneration. To determine the cells on which the AR subtypes were located, we dissociated cells from various regions of the adult rat brain and subsequently identified astrocytes by glial fibrillary acidic protein (GFAP) immunofluorescence. Slides containing the astrocytes were prepared for autoradiography using the nonselective beta ligand 125I-iodocyanopindolol (125ICYP) or the alpha 1 ligand 125IBE 2254 (125I-HEAT). The addition of the selective beta 1 blocker betaxolol or the beta 2 blocker ICI 118.551 to the incubation medium to displace 125ICYP binding was used to determine the binding of beta-AR subtypes. The great majority (greater than 88%) of isolated astrocytes sampled from the trigeminal motor nucleus, cerebral cortex, striatum, and cerebellum showed beta-AR binding. Astrocytes from the first three regions had similar average densities of beta-ARs, whereas the density in cerebellar astrocytes was 2- to 3-fold greater. The beta 2-AR subtype was proportionally greater than the beta 1 subtype in each region. Reactive astrocytes isolated from the trigeminal motor nucleus after degeneration of motor neurons showed a beta-AR density nearly 2-fold greater than resting astrocytes from the same region, with the beta 1 subtype showing the greater proportional increase. There was no beta-AR binding on trigeminal motor neurons. Astrocytes also showed a significant level of alpha 1-AR binding. No differences in alpha 1-AR binding were found in normal astrocytes isolated from the different regions, nor was there an increase in reactive astrocytes. In contrast, trigeminal motor neurons had an alpha 1-AR density nearly 10 times greater than astrocytes. In terms of the NE modulation of synaptic responses in motor neurons, the distribution of ARs would permit NE to act indirectly through alpha 1 and beta receptors on astrocytes and directly through alpha 1 receptors on motor neurons.
Shao
Y
Y
Department of Anatomy and Cell Biology, Emory University School of Medicine, Atlanta, Georgia 30322.
Sutin
J
J
D000818:Animals; D001253:Astrocytes / Q000378:metabolism*; D001345:Autoradiography; D001921:Brain / Q000166:cytology / Q000378:metabolism*; D002531:Cerebellum / Q000166:cytology / Q000378:metabolism; D002540:Cerebral Cortex / Q000166:cytology / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis / Q000276:immunology; D009046:Motor Neurons / Q000378:metabolism*; D009410:Nerve Degeneration; D009457:Neuroglia / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011941:Receptors, Adrenergic / Q000096:biosynthesis*; D011942:Receptors, Adrenergic, alpha / Q000096:biosynthesis / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000096:biosynthesis / Q000378:metabolism; D014276:Trigeminal Nerve / Q000166:cytology / Q000378:metabolism
D005904:Glial Fibrillary Acidic Protein; D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta