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      Expression of Corticotropin-Releasing Hormone Type 1 Receptor in Paraventricular Nucleus after Acute Stress

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          We have previously proposed the existence of ultrashort loop-positive feedback regulation of corticotropin-releasing hormone (CRH) in the hypothalamus. To gain a better understanding of this effect, we performed double-label in situ hybridization to identify the neurons in the paraventricular nucleus (PVN) that express CRH type 1 receptor (CRH-R1) following stress. We also conducted immunohistochemistry to determine whether CRH-R1 mRNA was translated to CRH-R1 protein in the PVN. Thirty-minute restraint stress given to male Wistar rats increased c- fos mRNA expression primarily in the CRH-producing neurons of the parvocellular PVN. Small numbers of vasopressin and oxytoxin-producing cells were also labeled by c- fos probes. Approximately 70% of CRH-R1 positive neurons exhibited CRH mRNA 2 h after the beginning of stress, while only a small percentage of the vasopressin and oxytocin-producing cells coexpressed CRH-R1 mRNA. CRH-R1 immunoreactivity, which was detected in the perikarya and fibers of PVN neurons, appeared to increase in response to stress, though this was not statistically significant. Pretreatment with a selective CRH-R1 antagonist, CP-154,526, significantly attenuated stress-induced corticotropin (ACTH) secretion as well as c- fos mRNA expression in the PVN. These results demonstrate that acute stress increases neuronal activation and CRH-R1 mRNA expression primarily in CRH-producing neurons of the parvocellular PVN, that CRH-R1 message is translated to CRH-R1 protein, and that PVN neurons are activated at least in part through CRH-R1 under acute stress. The data further support the possibility of feedback regulation of CRH itself in CRH-producing neurons.

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          Most cited references 5

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          Physiological and behavioral responses to corticotropin-releasing factor administration: is CRF a mediator of anxiety or stress responses?

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            Water-avoidance stress-induced c-fos expression in the rat brain and stimulation of fecal output: role of corticotropin-releasing factor.

             B Bonaz,  Y Taché (1994)
            Immunohistochemical detection of the immediate-early gene c-fos was used to determine the pattern of neuronal activity in the rat brain after exposure to water-avoidance stress known to stimulate fecal output in rats. Avoidance to water for 1 h by standing on a small platform increases pellet output and induces numerous Fos-positive cells in the parvocellular part of the paraventricular nucleus of the hypothalamus (PVN), locus coeruleus (LC) and, to a lesser extent, in the bed nucleus of the stria terminalis, lateral septum, dorsal raphe nucleus and A5 and A1 noradrenergic neurons. The corticotropin-releasing factor (CRF) antagonist, alpha-helical CRF9-41 (50 micrograms i.c.v.) reduced water-avoidance stress-induced c-fos expression mainly in the PVN and the LC (44 and 60%, respectively) and decreased by 60% the stimulated fecal output. These data indicate that water-avoidance stress activates PVN and LC neurons through CRF pathways which contribute to the stimulation of colonic motor function.
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              CP-154,526: a potent and selective nonpeptide antagonist of corticotropin releasing factor receptors.

              Here we describe the properties of CP-154,526, a potent and selective nonpeptide antagonist of corticotropin (ACTH) releasing factor (CRF) receptors. CP-154,526 binds with high affinity to CRF receptors (Ki < 10 nM) and blocks CRF-stimulated adenylate cyclase activity in membranes prepared from rat cortex and pituitary. Systemically administered CP-154,526 antagonizes the stimulatory effects of exogenous CRF on plasma ACTH, locus coeruleus neuronal firing and startle response amplitude. Potential anxiolytic activity of CP-154,526 was revealed in a fearpotentiated startle paradigm. These data are presented in the context of clinical findings, which suggest that CRF is hypersecreted in certain pathological states. We propose that a CRF antagonist such as CP-154,526 could affirm the role of CRF in certain psychiatric diseases and may be of significant value in the treatment of these disorders.

                Author and article information

                S. Karger AG
                May 2001
                31 May 2001
                : 73
                : 5
                : 293-301
                aDepartment of Bioregulation, Institute of Gerontology, Nippon Medical School, Kawasaki; bDepartment of Anatomy, Nippon Medical School, Tokyo, Departments of cPhysiology and dMedicine, Tokyo Women’s Medical University, Tokyo, and eLaboratory for Learning and Memory, Brain Science Institute, RIKEN, Wako, Japan
                54646 Neuroendocrinology 2001;73:293–301
                © 2001 S. Karger AG, Basel

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                Page count
                Figures: 6, References: 37, Pages: 9
                Stress, Corticotropin and Behaviour


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