AbstractAttempts 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 β‐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 β ligand125I‐iodocyanopindolol (125ICYP) or the α1ligand125IBE 2254 (125I‐HEAT). The addition of the selective β1blocker betaxolol or the β2blocker ICI 118.551 to the incubation medium to displace125ICYP binding was used to determine the binding of β‐AR subtypes.The great majority (>88) of isolated astrocytes sampled from the trigeminal motor nucleus, cerebral cortex, striatum, and cerebellum showed β‐AR binding. Astrocytes from the first three regions had similar average densities of β‐ARs, whereas the density in cerebellar astrocytes was 2‐ to 3‐fold greater. The β2‐AR subtypes was proportionally greater than the β1subtype in each region. Reactive astrocytes isolated from the trigeminal motor nucleus after degeneration of motor neurons showed a β‐AR density nearly 2‐fold greater than resting astrocytes from the same region, with the β1subtype showing the greater proportional increase. There was no β‐AR binding on trigeminal motor neurons.Astrocytes also showed a significant level of α1‐AR binding. No differences in α1‐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 α1‐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 α1and β receptors on astrocytes and directly through α1re
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