RATIONALE: Schizophrenia is a major public health problem that affects approximately 1% of the population worldwide. Schizophrenia-like syndromes can be induced in humans by phencyclidine (PCP), a drug with marked psychomimetic properties. Recent studies show that the behavioural and biochemical effects of PCP in rats are blocked by nitric oxide synthase (NOS) inhibitors, suggesting that NO plays an important role in the pharmacological effects of PCP. OBJECTIVE: The aim of this study was to investigate if PCP-induced disruption of prepulse inhibition of acoustic startle could be blocked by the NOS inhibitor, L-NAME, in mice. RESULTS: The present study shows that PCP readily disrupts prepulse inhibition in mice normally without affecting pulse-alone trials. Furthermore, L-NAME blocked the PCP-induced disruption of prepulse inhibition in a dose-related manner. CONCLUSIONS: The PCP-induced disruption of prepulse inhibition and the ability of L-NAME to block this effect in both rats and mice suggest that this is a general and not a species-specific effect. The results of the present study further suggest that PCP exerts at least some of its actions in the central nervous system by a NO-dependent mechanism.
RATIONALE: Schizophrenia is a major public health problem that affects approximately 1% of the population worldwide. Schizophrenia-like syndromes can be induced in humans by phencyclidine (PCP), a drug with marked psychomimetic properties. Recent studies show that the behavioural and biochemical effects of PCP in rats are blocked by nitric oxide synthase (NOS) inhibitors, suggesting that NO plays an important role in the pharmacological effects of PCP. OBJECTIVE: The aim of this study was to investigate if PCP-induced disruption of prepulse inhibition of acoustic startle could be blocked by the NOS inhibitor, L-NAME, in mice. RESULTS: The present study shows that PCP readily disrupts prepulse inhibition in mice normally without affecting pulse-alone trials. Furthermore, L-NAME blocked the PCP-induced disruption of prepulse inhibition in a dose-related manner. CONCLUSIONS: The PCP-induced disruption of prepulse inhibition and the ability of L-NAME to block this effect in both rats and mice suggest that this is a general and not a species-specific effect. The results of the present study further suggest that PCP exerts at least some of its actions in the central nervous system by a NO-dependent mechanism.
Authors: Daniel Klamer; Erik Pålsson; Kim Fejgin; Jianhua Zhang; Jörgen A Engel; Lennart Svensson Journal: Psychopharmacology (Berl) Date: 2004-12-24 Impact factor: 4.530
Authors: Kim Fejgin; Sergej Safonov; Erik Pålsson; Caroline Wass; Jörgen A Engel; Lennart Svensson; Daniel Klamer Journal: Psychopharmacology (Berl) Date: 2007-01-19 Impact factor: 4.530
Authors: Daniel Klamer; Erik Pålsson; Aron Revesz; Jörgen A Engel; Lennart Svensson Journal: Psychopharmacology (Berl) Date: 2004-06-02 Impact factor: 4.530
Authors: Ana C Issy; João Francisco C Pedrazzi; Bruno H Yoneyama; Elaine A Del-Bel Journal: Psychopharmacology (Berl) Date: 2013-10-08 Impact factor: 4.530
Authors: Nicole L Roenker; Gary A Gudelsky; Rebecca Ahlbrand; Paul S Horn; Neil M Richtand Journal: Neuropharmacology Date: 2012-05-09 Impact factor: 5.250