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  • Wass, Caroline,1976Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi,Institute of Neuroscience and Physiology, Department of Pharmacology (author)

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

  • Article/chapterEnglish2008

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  • Elsevier BV,2008

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  • LIBRIS-ID:oai:gup.ub.gu.se/81157
  • https://gup.ub.gu.se/publication/81157URI
  • https://doi.org/10.1016/j.pbb.2008.01.011DOI

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  • Language:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

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  • 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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  • Svensson, Lennart,1952Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi,Institute of Neuroscience and Physiology, Department of Pharmacology(Swepub:gu)xsvenl (author)
  • Fejgin, Kim,1978Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi,Institute of Neuroscience and Physiology, Department of Pharmacology(Swepub:gu)xfejki (author)
  • Pålsson, Erik,1975Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi,Institute of Neuroscience and Physiology, Department of Pharmacology(Swepub:gu)xpaler (author)
  • Archer, Trevor,1949Gothenburg University,Göteborgs universitet,Psykologiska institutionen,Department of Psychology(Swepub:gu)xarctr (author)
  • Engel, Jörgen,1942Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi,Institute of Neuroscience and Physiology, Department of Pharmacology(Swepub:gu)xenjor (author)
  • Klamer, Daniel,1976Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi,Institute of Neuroscience and Physiology, Department of Pharmacology(Swepub:gu)xklada (author)
  • Göteborgs universitetInstitutionen för neurovetenskap och fysiologi, sektionen för farmakologi (creator_code:org_t)

Related titles

  • In:Pharmacology, biochemistry, and behavior: Elsevier BV89:3, s. 352-90091-3057

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