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Nitric oxide synthase inhibition attenuates phencyclidine-induced disruption of cognitive flexibility.

Journal article
Authors Caroline Wass
Lennart Svensson
Kim Fejgin
Erik Pålsson
Trevor Archer
Jörgen Engel
Daniel Klamer
Published in Pharmacology, biochemistry, and behavior
Volume 89
Issue 3
Pages 352-9
ISSN 0091-3057
Publication year 2008
Published at Department of Psychology
Institute of Neuroscience and Physiology, Department of Pharmacology
Pages 352-9
Language en
Keywords Animals, Cognition, drug effects, Enzyme Inhibitors, pharmacology, Male, NG-Nitroarginine Methyl Ester, pharmacology, Nitric Oxide, biosynthesis, Nitric Oxide Synthase, antagonists & inhibitors, Phencyclidine, pharmacology, Rats, Rats, Sprague-Dawley, Stereotyped Behavior, drug effects, Swimming
Subject categories Pharmacology and Toxicology


Schizophrenia encompasses, amongst other symptoms, a heavy load of cognitive dysfunctionality. Using the psychotomimetic agent, phencyclidine (PCP), we have previously found that PCP-induced disruptions of cognitive function in translational rodent models of schizophrenia are dependent on nitric oxide (NO) production. In the present study, male Sprague-Dawley rats were subjected to a Morris water maze task designed to assess cognitive flexibility (i.e. the ability to cope with an increasingly demanding cognitive task) by means of a "constant reversal learning paradigm". Experiments were conducted to evaluate the effects of the NO synthase inhibitor, L-NAME (10 mg/kg), on PCP-induced (2 mg/kg) impairments. Control animals significantly improved their learning over the first 3 consecutive days, whereas PCP-treated animals failed to show any significant learning. Pretreatment with L-NAME normalized the PCP-induced disruption of learning to control levels. These findings suggest that PCP-induced disruptions of cognitive flexibility (i.e. ability to modify behaviour according to an increasingly demanding cognitive task) are dependent upon NO production. These observations, together with accumulated clinical findings, suggest that the NO system is a potential treatment target for cognitive dysfunctions in schizophrenia.

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