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Phencyclidine-induced behaviour in mice prevented by methylene blue
Daniel Klamer1, Jörgen A Engel, Lennart Svensson
1Department of Pharmacology, Göteborg University, Göteborg, Sweden.
Basic & Clinical Pharmacology & Toxicology
|January 30, 2004
Summary
Methylene blue reversed phencyclidine-induced disruptions in prepulse inhibition and hyperlocomotion in mice, suggesting nitric oxide synthase inhibition may treat schizophrenia.
Area of Science:
- Neuroscience
- Pharmacology
- Psychiatry
Background:
- Schizophrenia affects 1% of the global population, presenting a significant public health challenge.
- Phencyclidine (PCP) induces schizophrenia-like symptoms and disrupts prepulse inhibition, a measure also impaired in schizophrenic patients.
- Nitric oxide synthase (NOS) inhibitors block PCP's effect on prepulse inhibition, implicating nitric oxide (NO) in PCP's actions.
Purpose of the Study:
- To investigate the effect of methylene blue, a NOS inhibitor, on phencyclidine-induced disruption of prepulse inhibition in mice.
- To examine methylene blue's impact on phencyclidine-induced hyperlocomotion.
Main Methods:
- Mice were administered phencyclidine (4 mg/kg) and varying doses of methylene blue (50 or 100 mg/kg).
- Prepulse inhibition of acoustic startle and locomotor activity were measured to assess behavioral effects.
Main Results:
- Phencyclidine disrupted prepulse inhibition in mice.
- Methylene blue dose-dependently prevented the phencyclidine-induced decrease in prepulse inhibition.
- Methylene blue pretreatment reduced phencyclidine-induced hyperlocomotion.
Conclusions:
- The findings support the involvement of the nitric oxide synthase/guanylate cyclase pathway in phencyclidine's behavioral and psychotomimetic effects.
- Agents targeting this pathway may hold therapeutic potential for schizophrenia treatment.
