Brain and pituitary receptors for corticotropin releasing factor: Localization and differential regulation after adrenalectomy

Behavioral and Anatomical Interactions between Dopamine and Corticotropin-Releasing Factor in the Rat

“…The BST is rich in CRF-containing neurons and CRF 1 receptors (Wynn et al, 1984), and chemical lesions of the BST (comprising both the dorsal and ventral BST) completely block CRFenhanced startle . Although intra-BST CRF only partially mimics the intracerebroventricular CRF effects on startle, and intra-BST infusion of a CRF antagonist does not completely block CRF-enhanced startle, the results from Lee and Davis (1997) strongly suggest that the BST is a critical site mediating CRF-enhanced startle.…”

International Union of Pharmacology. XXXVI. Current Status of the Nomenclature for Receptors for Corticotropin-Releasing Factor and Their Ligands

“…Initially, the action of CRF appeared to be restricted to regulating ACTH secretion by pituitary corticotrope cells (Vale et al, 1981;Dunn and Berridge 1990;Hauger and Dautzenberg, 1999;Smagin et al, 2001). The central distribution of CRF pathways, however, suggested that CRF's function extended far beyond the classical action of a hormone (Swanson et al, 1983;De Souza et al, 1984;Wynn et al, 1984;Vale et al, 1997;Arborelius et al, 1999;Heinrichs and De Souza 1999;Dautzenberg et al, 2001a). Because CRF was shown to generate neuroendocrine, autonomic, and behavioral stress responses, it was hypothesized that CRF contributed to the development of stress and affective disorders by over-activating its receptors expressed in various brain neurons in neocortex, the amygdala and its extended neurocircuits, and brainstem nuclei.…”

Restraint-stress-induced changes in exploratory behavior appear to be mediated by norepinephrine-stimulated release of CRF

“…This research was supported by the National Institute of Mental Health (MH25486) and a fellowship to C. When released from the median eminence of the hypothalamus, corticotropin-releasing factor (CRF) is a critical regulator of the glucocorticoid response in stress. However, CRF (Swanson et al, 1983) and high-affinity binding sites for CRF have been identified in many areas of the brain (Wynn et al, 1984), and a Ca2+-dependent release of CRF was observed in many of these regions (Smith et al, 1986). When injected directly into the brain, CRF elicits a number of neurochemical, physiological, and behavioral responses that resemble those observed in stress Morley and Levine, 1982;Sutton et al, 1982;Kalin et al, 1983;Berridge and Dunn, 1986;Dunn and Berridge, 1987).…”