Distribution of mRNAs encoding CRF receptors in brain and pituitary of batand mouse

Two G protein-coupled receptors have been identified that bind corticotropi n-releasing factor (CRF) and urocortin (UCN) with high affinity. Hybridizat ion histochemical methods were used to shed light on controversies concerni ng their localization in rat brain, and to provide normative distributional data in mouse, the standard model for genetic manipulation in mammals. The distribution of CRF-R1 mRNA in mouse was found to be fundamentally similar to that in rat, with expression predominating in the cerebral cortex, sens ory relay nuclei, and in the cerebellum and its major afferents. Pronounced species differences in distribution were few, although more subtle variati ons in the relative strength of R1 expression were seen in several forebrai n regions. CRF-RB mRNA displayed comparable expression in rat and mouse bra in, distinct from, and more restricted than that of CRF-R1. Major neuronal sites of CRF-RB expression included aspects of the olfactory bulb, lateral septal nucleus, bed nucleus of the stria terminalis, ventromedial hypothala mic nucleus, medial and posterior cortical nuclei of the amygdala, ventral hippocampus, mesencephalic raphe nuclei, and novel localizations in the nuc leus of the solitary tract and area postrema. Several sites of expression i n the limbic forebrain were found to overlap partially with ones of androge n receptor expression. In pituitary, rat and mouse displayed CRF-R1 mRNA si gnal continuously over the intermediate lobe and over a subset of cells in the anterior lobe, whereas CRF-RB transcripts were expressed mainly in the posterior lobe. The distinctive expression pattern of CRF-RB mRNA identifie s additional putative central sites of action for CRF and/or UCN, Constitut ive expression of CRF-RS mRNA in the nucleus of the solitary tract, and str ess-inducible expression of CRF-R1 transcripts in the paraventricular nucle us may provide a basis for understanding documented effects of CRF-related peptides at a loci shown previously to lack a capacity for CRF-R expression or CRF binding. Other such "mismatches" remain to be reconciled. (C) 2000 Wiley-Liss, Inc.