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Effects of sodium benzoate on pre-pulse inhibition deficits and hyperlocomotion in mice after administration of phencyclidine

Published online by Cambridge University Press:  04 February 2015

Akiko Matsuura ,
Yuko Fujita ,
Masaomi Iyo  and
Kenji Hashimoto
Akiko Matsuura
Affiliation:
Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba, Japan Department of Psychiatry, Chiba University Graduate School of Medicine, Chiba, Japan
Yuko Fujita
Affiliation:
Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba, Japan
Masaomi Iyo
Affiliation:
Department of Psychiatry, Chiba University Graduate School of Medicine, Chiba, Japan
Kenji Hashimoto*
Affiliation:
Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba, Japan
*
Dr. Kenji Hashimoto, Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, 1-8-1 Inohana, Chiba 260-8670, Japan. Tel: +81-43-226-2517; Fax: +81-43-226-2561; E-mail: hashimoto@faculty.chiba-u.jp
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Abstract

Objective

A recent clinical study demonstrated that sodium benzoate (SB), a prototype competitive d-amino acid oxidase inhibitor, was effective in the treatment of several symptoms, such as positive and negative symptoms, and cognitive impairment in medicated patients with schizophrenia. The objective of the study was to examine the effects of SB on behavioural abnormalities such as pre-pulse inhibition (PPI) deficits and hyperlocomotion in mice after a single administration of the N-methyl-d-aspartate (NMDA) receptor antagonist, phencyclidine (PCP).

Methods

The effects of SB on behavioural abnormalities (PPI deficits and hyperlocomotion) in mice after PCP administration were examined. Furthermore, effects of SB on tissue levels of amino acids were also examined.

Results

A single oral dose of SB (100, 300, or 1000 mg/kg) attenuated PPI deficits in mice after administration of PCP (3.0 mg/kg, s.c.) in a dose-dependent manner. In contrast, L-701,324 (10 mg/kg), an antagonist at the glycine site of the NMDA receptor, did not affect the effect of SB (1000 mg/kg) on PCP-induced PPI deficits. Furthermore, a single oral dose of SB (1000 mg/kg) significantly attenuated the hyperlocomotion in mice after administration of PCP (3.0 mg/kg, s.c.). However, a single oral dose of SB (1000 mg/kg) caused no changes to d-serine levels in plasma or in the frontal cortex, hippocampus, and striatum of these animals.

Conclusion

This study suggests that SB induced antipsychotic effects in the PCP model of schizophrenia, although it did not increase d-serine levels in the brain.

Keywords

d-amino acid oxidased-serinephencyclidinesodium benzoate
Type
Original Articles
Information
Acta Neuropsychiatrica , Volume 27 , Issue 3 , June 2015 , pp. 159 - 167
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Copyright
© Scandinavian College of Neuropsychopharmacology 2015 

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