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

Free Radic Res. 2016;50(11):1245-1256. doi: 10.1080/10715762.2016.1234048. Epub 2016 Oct 12.

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; dopamine transporter; monoamine; oxidative stress; shuttle-box; sociability.

MeSH terms

  • Animals
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Oxidative Stress
  • Reactive Oxygen Species
  • Stress, Psychological
  • Superoxide Dismutase / genetics*
  • Superoxide Dismutase / metabolism
  • Synaptic Transmission

Substances

  • Reactive Oxygen Species
  • Superoxide Dismutase