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Corticotropin Releasing Factor (corticotropin + releasing_factor)
Selected AbstractsDifferential effects of stress and amphetamine administration on Fos-like protein expression in corticotropin releasing factor-neurons of the rat brainDEVELOPMENTAL NEUROBIOLOGY, Issue 6 2007David Rotllant Abstract Corticotropin releasing factor (CRF) appears to be critical for the control of important aspects of the behavioral and physiological response to stressors and drugs of abuse. However, the extent to which the different brain CRF neuronal populations are similarly activated after stress and drug administration is not known. We then studied, using double immunohistochemistry for CRF and Fos protein, stress and amphetamine-induced activation of CRF neurons in cortex, central amygdala (CeA), medial parvocellular dorsal, and submagnocellular parvocellular regions of the paraventricular nucleus of the hypothalamus (PVNmpd and PVNsm, respectively) and Barrington nucleus (Bar). Neither exposure to a novel environment (hole-board, HB) nor immobilization (IMO) increased Fos-like immunoreactivity (FLI) in the CeA, but they did to the same extent in cortical regions. In other regions only IMO increased FLI. HB and IMO both failed to activate CRF+ neurons in cortical areas, but after IMO, some neurons expressing FLI in the PVNsm and most of them in the PVNmpd and Bar were CRF+. Amphetamine administration increased FLI in cortical areas and CeA (with some CRF+ neurons expressing FLI), whereas the number of CRF+ neurons increased only in the PVNsm, in contrast to the effects of IMO. The present results indicate that stress and amphetamine elicited a distinct pattern of brain Fos-like protein expression and differentially activated some of the brain CRF neuronal populations, despite similar levels of overall FLI in the case of IMO and amphetamine. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007. [source] Central Administration of Orexin A Suppresses Basal and Domperidone Stimulated Plasma ProlactinJOURNAL OF NEUROENDOCRINOLOGY, Issue 12 2000S. H. Russell Abstract Orexin immunoreactive fibres are abundant in the hypothalamus suggesting a neuroendocrine regulatory role. Intracerebroventricular (ICV) administration of orexin A suppressed plasma prolactin in male rats by 71% at 20 min post-injection and 83% at 90 min post-injection (P < 0.005 vs saline at both time points). To investigate whether this effect was through the tuberoinfundibular dopaminergic (TIDA) system, a supra-maximal dose of domperidone, a dopamine receptor antagonist, was injected intraperitoneally (i.p.) prior to ICV injection of orexin A. ICV orexin A significantly suppressed domperidone (9 mg/kg)-stimulated plasma prolactin levels, by up to 40% (i.p. domperidone + ICV orexin A 3 nmol 34.5 ± 7.4 ng/ml and i.p. domperidone + ICV orexin A 20 nmol 43.5 ± 4.3 ng/ml, both P < 0.005 vs i.p. domperidone + ICV saline 57.9 ± 2.7 ng/ml). Orexin A, 100 nM, significantly stimulated release of neurotensin, vasoactive intestinal polypeptide, somatostatin, corticotropin releasing factor and luteinizing hormone releasing hormone, but had no effect on release of dopamine, thyrotropin releasing hormone (TRH), vasopressin or melanin-concentrating hormone from hypothalamic explants in vitro. Orexin A did not alter basal or TRH stimulated prolactin release in dispersed pituitary cells harvested from male rats. The data suggest that ICV administration of orexin A suppresses plasma prolactin in part through a pathway independent of the dopaminergic system. [source] Blockade of the Corticotropin Releasing Factor Type 1 Receptor Attenuates Elevated Ethanol Drinking Associated With Drinking in the Dark ProceduresALCOHOLISM, Issue 2 2008Dennis R. Sparta Background:, Drinking in the dark (DID) procedures have recently been developed to induce high levels of ethanol drinking in C57BL/6J mice, which result in blood ethanol concentrations (BECs) reaching levels that have measurable affects on physiology and/or behavior. The present experiments determined whether the increased ethanol drinking caused by DID procedures can be attenuated by pretreatment with CP-154,526; a corticotropin releasing factor type-1 (CRF1) receptor antagonist. Methods:, In Experiment 1, male C57BL/6J mice received ethanol (20% v/v) in place of water for 4 hours, beginning with 3 hours into the dark cycle. On the fourth day, mice were given an intraperitoneal injection of one of the 4 doses of CP-154,526 (0, 1, 3, 10 mg/kg) 30 minutes before receiving their ethanol bottle. In Experiment 2, C57BL/6J mice had 2 hours of access to the 20% ethanol solution, beginning with 3 hours into the dark cycle on days 1 to 3, and 4 hours of access to the ethanol bottle on day 4 of DID procedures. Mice were given an intraperitoneal injection of one of the 4 doses of CP-154,526 (0, 1, 3, 10 mg/kg) 30 minutes before receiving their ethanol bottle on day 4. Tail blood samples were collected immediately after the 4-hour ethanol access period on the fourth day of each experiment. Additional control experiments assessed the effects of CP-154,526 on 4-hour consumption of a 10% (w/v) sucrose solution and open-field locomotor activity. Results:, In Experiment 1, the vehicle-treated group consumed approximately 4.0 g/kg/4 h of ethanol and achieved BECs of approximately 30 mg%. Furthermore, pretreatment with the CRF1 receptor antagonist did not alter ethanol consumption. On the other hand, procedures used in Experiment 2 resulted in vehicle-treated mice consuming approximately 6.0 g/kg/4 h of ethanol with BECs of about 80 mg%. Additionally, the 10 mg/kg dose of CP-154,526 significantly reduced ethanol consumption and BECs to approximately 3.0 g/kg/4 h and 27 mg%, respectively, relative to vehicle-treated mice. Importantly, the 10 mg/kg dose of the CRF1R antagonist did not significantly alter 4-hour sucrose consumption or locomotor activity. Conclusions:, These data indicate that CRF1R signaling modulates high, but not moderate, levels of ethanol drinking associated with DID procedures. [source] Over-Expression of Neuropeptide Urocortin and Its Receptors in Human Allergic Nasal Mucosa,THE LARYNGOSCOPE, Issue 9 2007Tae Hoon Kim MD Abstract Objectives: Urocortin (UCN) is a member of the corticotropin releasing factor (CRF) neuropeptide family. UCN act as locally expressed proinflammatory factor and induce mast cell degranulation, cytokine secretion, and trigger vascular permeability, which are mediated by CRF receptors in peripheral tissues. Considering its functional roles, UCN and its receptors may play a role in the pathogenesis of allergic nasal mucosa. Therefore, we investigated the expression profile and distribution of UCN and CRF receptors in normal and allergic nasal mucosa. Methods: Reverse transcriptase-polymerase chain reaction, immunohistochemistry, and Western blotting were applied to the normal and allergic nasal mucosa. Results: The expression levels of UCN and CRF receptors were increased in allergic nasal mucosa in comparison with normal nasal mucosa. In normal nasal mucosa, UCN and CRF receptors were restricted to the vascular endothelium of submucosal cavernous sinusoids where faint staining was found. However, in allergic nasal mucosa, UCN was expressed in small vessels distributed in lamina propria and the vascular endothelium of cavernous sinusoid located in submucosa. Many scattered positive cells were also found in allergic nasal mucosa, probably UCN-positive leukocytes. CRF receptors were also localized in the vascular endothelium of small vessels and cavernous sinusoid. Conclusions: These results indicate that UCN may play a role in the regulation of vascular swelling in normal nasal mucosa. Moreover, in allergic nasal mucosa, increased expression levels of UCN and its receptors may contribute to increased mucosal swelling and vascular permeability, playing an important role in the pathogenesis of allergic rhinitis. [source] | ||||||||||