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ILR Genetics Consortium Emerging Risk Factors Collaboration Sarwar N Butterworth AS Freitag DF Gregson J Willeit P Gorman DN Gao P Saleheen D Rendon A Nelson CP Braund PS Hall AS Chasman DI Tybjærg-Hansen A Chambers JC Benjamin EJ Franks PW Clarke R Wilde AA Trip MD Steri M Witteman JC Qi L van der Schoot CE de Faire U Erdmann J Stringham HM Koenig W Rader DJ Melzer D Reich D Psaty BM Kleber ME Panagiotakos DB Willeit J Wennberg P Woodward M Adamovic S Rimm EB Meade TW Gillum RF Shaffer JA 《Lancet》2012,379(9822):1205-1213
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X M Yang A L Gorman A J Dunn 《The Journal of pharmacology and experimental therapeutics》1990,255(3):1064-1070
The role of the central noradrenergic systems and corticotropin-releasing factor (CRF) in modulating defensive withdrawal behavior was studied in rats. The apparatus consisted of a small chamber set on one side of a one-meter open field, into which the rat was placed to start the test. When rats were unfamiliar with the apparatus, they displayed species typical defensive withdrawal behavior with long latencies to emerge from and a high proportion of time spent in the small chamber. Intraperitoneal administration of clonidine (0.03 mg/kg), l-propranolol (2.5 micrograms/kg), prazosin (0.1 mg/kg) or chlordiazepoxide (CDP, 5 mg/kg) each significantly decreased the latency to emerge from and the mean time spent in the small chamber (MTIC) and increased the number of chamber entries. When rats were familiar with the apparatus, prior restraint for 20 min significantly increased the latency and MTIC, and decreased the number of chamber entries and rears, but did not alter locomotor activity. Prazosin, clonidine, CDP, l-propranolol and the CRF-antagonist, alpha-helical CRF9-41 (25 micrograms i.c.v.), reversed the restraint-induced increase in the latency and MTIC. CRF (10-100 ng i.c.v.) dose-dependently induced defensive withdrawal behavior in rats familiar with the apparatus; the minimum statistically significant dose was 50 ng. dl-Propranolol (5 mg/kg) and CDP blocked the CRF-induced changes in the latency to emerge and the MTIC; whereas clonidine and prazosin significantly reduced the latency, but had no statistically significant effects on the MTIC. Phenylephrine (25-200 ng i.c.v.) dose-dependently induced defensive withdrawal behavior. This effect of phenylephrine (200 ng) was significantly antagonized by prazosin or alpha-helical CRF9-41 (25 or 50 mg i.c.v.), but not by CDP. Our results suggest that the hyperactivity of the central noradrenergic systems caused by exposure to the novel environment may stimulate the release of CRF, which through some unknown mechanism induces defensive withdrawal behavior in rats. Activation of beta adrenergic receptors may also induce defensive withdrawal. 相似文献
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