The absence of the SOD1 gene causes abnormal monoaminergic neurotransmission and motivational impairment-like behavior in mice

Abstract

Copper/zinc superoxide dismutase (SOD1), a primary anti-oxidative enzyme, protects cells against oxidative stress. We report herein on a comparison of behavioral and neurobiological changes between SOD1 knockout (KO) and wild-type mice, in an attempt to assess the role of SOD1 in brain functions. SOD1 KO mice exhibited impaired motivational behavior in both shuttle-box learning and three-chamber social interaction tests. High levels of dopamine transporter protein and an acceleration of serotonin turnover were also detected in the cerebrums of the SOD1 KO mice. These findings suggest that SOD1 deficiency disturbs monoaminergic neurotransmission leading to a decrease in motivational behavior.

Keywords:

• SOD1
• oxidative stress
• shuttle-box
• sociability
• monoamine
• dopamine transporter

Acknowledgements

We sincerely appreciate Dr. Hiroyuki Iso for instructions in behavioral testing and related valuable suggestions.

Disclosure statement

The authors declare that there is no conflict of interest.

Funding

This work was supported by Grant-in-Aid for Researchers, Hyogo College of Medicine, 2012 and JSPS KAKENHI [grant Nos. 15K16534 and 24500877].