These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: The effect of corticotropin-releasing factor on prepulse inhibition is independent of serotonin in Brown Norway and Wistar-Kyoto rats. Author: Sutherland JE, Page ME, Conti LH. Journal: Pharmacol Biochem Behav; 2008 May; 89(3):324-37. PubMed ID: 18280562. Abstract: Prepulse inhibition (PPI), a form of sensorimotor gating, is reduced in a number of psychiatric disorders. Two experiments were conducted to determine whether corticotropin-releasing factor (CRF), which decreases PPI, does so via effects on serotonin (5-HT). Wistar-Kyoto (WKY) and Brown Norway (BN) rats were used in both experiments in order to examine whether strain-dependent differences would be apparent in response to manipulations of the CRF and 5-HT systems. In the first experiment, WKY and BN rats received a subcutaneous injection of the 5-HT(2A/C) receptor antagonist, ketanserin (2.0 mg/kg). Ten minutes later, rats received an intracerebroventricular (ICV) infusion of either 6.0 microl saline or CRF (0.3 microg or 3.0 microg). CRF decreased PPI despite blockade of 5-HT(2A/C) receptors with ketanserin. In the second experiment, WKY and BN rats received an intraperitoneal injection of the 5-HT synthesis inhibitor, p-chlorophenylalanine (PCPA, 150 mg/kg), 48 and 24 h prior to testing. On testing day, rats received an ICV infusion of either 6.0 microl saline or CRF (0.3 microg or 3.0 microg). CRF decreased PPI despite 5-HT depletion. These findings suggest that CRF does not decrease PPI via effects on 5-HT, since neither blockade of 5-HT(2A/C) receptors nor 5-HT depletion attenuated this decrease.[Abstract] [Full Text] [Related] [New Search]