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Distribution of α1A adrenergic receptor m RNA in the rat brain visualized by in situ hybridization

Norepinephrine has been implicated in a number of physiological, behavioral, and cellular modulatory processes in the brain, and many of these modulatory effects are attributable to α1 adrenergic receptors. At least three α1 receptor subtypes have been identified by molecular criteria, designated α1A, α1B, and α1D. The distributions of α1B and α1D receptor mRNA expression in rat brain have been described previously, but the cDNA for the rat α1A receptor has only recently been cloned and characterized. In the present study, we used a radiolabelled riboprobe derived from the rat α1A receptor cDNA to describe the distribution of α1A message expression in the rat brain. The highest levels of α1A adrenergic receptor mRNA expression were seen in the olfactory bulb, tenia tectae, horizontal diagonal band/magnocellular preoptic area, zona incerta, ventromedial hypothalamus, lateral mammillary nuclei, ventral dentate gyrus, piriform cortex, medial and cortical amygdala, magnocellular red nuclei, pontine nuclei, superior and lateral vestibular nuclei, brainstem reticular nuclei, and several cranial nerve motor nuclei. Dual in situ hybridization combining a radioactive riboprobe for choline acetyltransferase mRNA with a digoxigenin‐labeled α1A riboprobe in the fifth and seventh cranial nerve motor nuclei showed that the α1A mRNA is expressed in cholinergic motor neurons. Prominent α1A hybridization signal was also seen in the neocortex, claustrum, lateral amygdala, ventral cochlear nucleus, raphe magnus, and in the ventral horn of thoracic spinal cord. This overall pattern of expression, considered in comparison with that previously described for the other α1 adrenergic receptor subtypes, may shed light on the different roles of the α1 receptors in mediating the neuromodulatory effects of norepinephrine in processes such as arousal, neuroendocrine control, sensorimotor regulation, and the stress response. J. Comp. Neurol. 386:358‐378, 1997. © 1997 Wiley‐Liss, Inc.