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Increased cortical nitric oxide release after phencyclidine administration.

Journal article
Authors Erik Pålsson
Niall Finnerty
Kim Fejgin
Daniel Klamer
Caroline Wass
Lennart Svensson
John Lowry
Published in Synapse (New York, N.Y.)
Volume 63
Issue 12
Pages 1083-1088
ISSN 1098-2396
Publication year 2009
Published at Institute of Neuroscience and Physiology, Department of Pharmacology
Pages 1083-1088
Language en
Keywords rat, schizophrenia, in vivo voltammetry, cognition
Subject categories Physiology


Phencyclidine exerts psychotomimetic effects in humans and is used as a pharmacological animal model for schizophrenia. We, and others, have demonstrated that phencyclidine induces cognitive deficits in rats that are associated with schizophrenia. These cognitive deficits can be normalized by inhibition of nitric oxide synthase. The development of selective microelectrochemical nitric oxide sensors may provide direct evidence for the involvement of nitric oxide in these effects. The aim of the present study was to use LIVE (long term in vivo electrochemistry) to investigate the effect of phencyclidine, alone or in combination with the nitric oxide synthase inhibitor L-NAME, on nitric oxide levels in the medial prefrontal cortex of freely moving rats. Phencyclidine (2 mg kg(-1)) produced an increase in cortical nitric oxide levels and this increase was ameliorated by L-NAME (10 mg kg(-1)). Tentatively, the results from the present study provide a biochemical rationale for the involvement of nitric oxide in the phencyclidine model of schizophrenia. Synapse 63:1083-1088, 2009. (c) 2009 Wiley-Liss, Inc.

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