ArticlePsychopharmacology2010
Information processing deficits and nitric oxide signalling in the phencyclidine model of schizophrenia.
Article in Psychopharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Role of nitric oxide and related molecules in schizophrenia pathogenesis: biochemical, genetic and clinical aspects.Frontiers in physiology · 2015Review
- Metaplastic effects of subanesthetic ketamine on CA1 hippocampal function.Neuropharmacology · 2014Article
- Evidence for involvement of nitric oxide and GABA(B) receptors in MK-801- stimulated release of glutamate in rat prefrontal cortex.Neuropharmacology · 2012Article
- Nitric oxide synthase mediation of darbepoetin's cognitive benefits: a paradoxical effect?Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleSchizophrenia-like cognitive deficits induced by phencyclidine (PCP), a drug commonly used to model schizophrenia in experimental animals, are attenuated by nitric oxide (NO) synthase inhibitors. Furthermore, PCP increases NO levels and sGC/cGMP signalling in the prefrontal cortex in rodents. Hence, a cortical NO/sGC/cGMP signalling pathway may constitute a target for novel pharmacological therapies in schizophrenia.
objectivesThe objective of this study was to further investigate the role of NO signalling for a PCP-induced deficit in pre-attentive information processing. MATERIALS AND
methodsMale Sprague-Dawley rats were surgically implanted with NO-selective amperometric microsensors aimed at the prefrontal cortex, ventral hippocampus or nucleus accumbens, and NO levels and prepulse inhibition (PPI) were simultaneously assessed.
resultsPCP treatment increased NO levels in the prefrontal cortex and ventral hippocampus, but not in the nucleus accumbens. The increase in NO levels was not temporally correlated to the deficit in PPI induced by PCP. Furthermore, pretreatment with the neuronal NO synthase inhibitor N-propyl-L-arginine dose-dependently attenuated both the increase in prefrontal cortex NO levels and the deficit in PPI.
conclusionsThese findings support a demonstrated role of NO in the behavioural and neurochemical effects of PCP. Furthermore, this effect is brain region-specific and mainly involves the neuronal isoform of NOS. However, a temporal correlation between a PCP-induced disruption of PPI and an increase in prefrontal cortex NO levels was not demonstrated, suggesting that the interaction between PCP and the NO system is more complex than previously thought.
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