Modulation of central nervous system actions of corticotropin-releasing factor by dynorphin-related peptides
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Cited by (28)
Stress and endocrine physiology
2018, Encyclopedia of Endocrine DiseasesRole of the kappa-opioid receptor system in stress-induced reinstatement of nicotine seeking in rats
2014, Behavioural Brain ResearchCitation Excerpt :Furthermore, KOR antagonism/gene deletion has previously been shown to block CRF-induced anxiety-like behavior [35,42]. There is also evidence to suggest directionality of the CRF/DYN interaction in the reverse since KOR activation also stimulates the release of CRF [107,108] and KOR agonist-induced reinstatement of cocaine [33] and alcohol [52] seeking can be blocked with a CRF antagonist. To help elucidate the nature of this relationship, future studies in our lab will investigate whether U50,488-induced reinstatement of nicotine seeking can be blocked with a CRF antagonist and conversely, whether CRF-induced reinstatement of nicotine seeking can be blocked with nor-BNI.
Protracted withdrawal from ethanol and enhanced responsiveness stress: Regulation via the dynorphin/kappa opioid receptor system
2013, AlcoholCitation Excerpt :KOR agonists stimulate the hypothalamic–pituitary–adrenal (HPA) axis in rodents (Laorden, Fuertes, Gonzalez-Cuello, & Milanes, 2000) and humans (Ur, Wright, Bouloux, & Grossman, 1997), which is primarily regulated by CRF release in the hypothalamus (Vale et al., 1983). DYN has also been found to modulate the effects of CRF on autonomic function (Overton & Fisher, 1989). In the basolateral amygdala, CRF increases KOR immunoreactivity (Bruchas et al., 2009; Land et al., 2008).
Corticotropin-releasing factor receptors and urocortins, links between the brain and the heart
2010, European Journal of PharmacologyOrganization and Integration of the Endocrine System: The Arousal and Sleep Perspective
2007, Sleep Medicine ClinicsCitation Excerpt :Autoregulatory ultrashort negative feedback loops are also present in both the PVN CRH and brain stem noradrenergic neurons [14,15], with collateral fibers inhibiting CRH and catecholamine secretion through presynaptic CRH and α2-noradrenergic receptors, respectively [14–16]. Both CRH and catecholaminergic neurons also receive stimulatory innervation from the serotonergic and cholinergic systems [17,18] and inhibitory input from the gamma-aminobutyric acid/benzodiazepine and opioid peptide neuronal systems of the brain [14,19,20] as well as through the end-product of the HPA axis, the glucocorticoids [14,21]. The secretion of CRH, a major anorexigenic peptide, is stimulated by neuropeptide Y (NPY), a potent known orexigenic factor, which simultaneously inhibits the LC/NE-sympathetic system [21–25].