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Related Experiment Videos

Phencyclidine affects memory in a nitric oxide-dependent manner: working and reference memory.

Caroline Wass1, Trevor Archer, Erik Pålsson

  • 1Department of Pharmacology, The Sahlgrenska Academy at Göteborg University, POB 431, SE 405 30 Göteborg, Sweden.

Behavioural Brain Research
|August 29, 2006
PubMed
Summary

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Phencyclidine (PCP) impairs spatial learning and memory in rats. However, L-NAME, a nitric oxide synthase inhibitor, reversed these cognitive deficits, suggesting a role for nitric oxide in PCP-induced memory dysfunction.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Cognitive Science

Background:

  • Schizophrenia is associated with cognitive deficits, particularly in learning and memory.
  • Phencyclidine (PCP) is a non-competitive NMDA receptor antagonist used to model schizophrenia-like cognitive dysfunction.
  • Nitric oxide (NO) plays a role in synaptic plasticity and memory processes.

Purpose of the Study:

  • To investigate the effects of PCP on working and reference memory in rats.
  • To determine if inhibiting nitric oxide synthase with L-NAME can ameliorate PCP-induced cognitive impairments.
  • To explore the role of nitric oxide in spatial memory deficits induced by PCP.

Main Methods:

  • Male Sprague-Dawley rats were used in a Morris water maze task to assess spatial learning and memory.

Related Experiment Videos

  • PCP (2.0 mg/kg) was administered to induce cognitive deficits.
  • L-NAME (10 mg/kg), a nitric oxide synthase inhibitor, was used as a pre-treatment.
  • A modified protocol distinguished between working and reference memory acquisition and retention.
  • Main Results:

    • PCP significantly disrupted the acquisition of both working and reference spatial memory.
    • Pre-treatment with L-NAME effectively reversed the memory impairments caused by PCP.
    • L-NAME alone did not significantly affect spatial memory acquisition or retention.

    Conclusions:

    • PCP-induced deficits in spatial learning and memory are mediated, at least in part, by mechanisms involving nitric oxide synthase.
    • Inhibition of nitric oxide synthase may represent a potential therapeutic strategy for cognitive dysfunction in conditions like schizophrenia.
    • This study highlights the complex interplay between NMDA receptor function, nitric oxide signaling, and cognitive processes.