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Catecholaminergic neuronal network dysfunction in the frontal lobe of a genetic mouse model of schizophrenia

Published online by Cambridge University Press:  03 September 2015

Shuji Iritani*
Affiliation:
Department of Psychiatry, Graduate School of Medicine, Nagoya University, Showa-ku, Nagoya, Aichi, Japan
Hirotaka Sekiguchi
Affiliation:
Department of Psychiatry, Graduate School of Medicine, Nagoya University, Showa-ku, Nagoya, Aichi, Japan
Chikako Habuchi
Affiliation:
Department of Psychiatry, Graduate School of Medicine, Nagoya University, Showa-ku, Nagoya, Aichi, Japan
Youta Torii
Affiliation:
Department of Psychiatry, Graduate School of Medicine, Nagoya University, Showa-ku, Nagoya, Aichi, Japan
Keisuke Kuroda
Affiliation:
Department of Cell Pharmacology, Graduate School of Medicine, Nagoya University, Showa-ku, Nagoya, Aichi, Japan
Kozo Kaibuchi
Affiliation:
Department of Cell Pharmacology, Graduate School of Medicine, Nagoya University, Showa-ku, Nagoya, Aichi, Japan
Norio Ozaki
Affiliation:
Department of Psychiatry, Graduate School of Medicine, Nagoya University, Showa-ku, Nagoya, Aichi, Japan
*
Shuji Iritani, Department of Psychiatry, Nagoya University Graduate School of Medicine, Tsurumai 65, Shouwa, Nagoya, Aichi 466-8550, Japan. Tel: +8 152 744 2282; Fax: +8 152 744 2293; E-mail: iritani@med.nagoya-u.ac.jp

Abstract

Background

The precise aetiology of schizophrenia remains unclear. The neurodevelopmental hypothesis of schizophrenia has been proposed based on the accumulation of genomic or neuroimaging studies.

Objective

In this study, we examined the catecholaminergic neuronal networks in the frontal cortices of disrupted-in-schizophrenia 1 (DISC1) knockout (KO) mice, which are considered to be a useful model of schizophrenia.

Methods

Six DISC1 homozygous KO mice and six age-matched littermates were used. The animals’ brains were cut into 20-μm-thick slices, which were then immunohistochemically stained using an anti-tyrosine hydroxylase (TH) monoclonal antibody.

Results

The TH-immunopositive fibres detected in the orbitofrontal cortices of the DISC1 KO mice were significantly shorter than those seen in the wild-type mice.

Conclusion

These neuropathological findings indicate that the hypofrontal symptoms of schizophrenia are associated with higher mental function deficiencies or cognitive dysfunction such as a loss of working memory.

Type
Short Communications
Copyright
© Scandinavian College of Neuropsychopharmacology 2015 

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