Morc1 knockout evokes a depression-like phenotype in mice

Behav Brain Res. 2016 Jan 1:296:7-14. doi: 10.1016/j.bbr.2015.08.005. Epub 2015 Aug 11.

Abstract

Morc1 gene has recently been identified by a DNA methylation and genome-wide association study as a candidate gene for major depressive disorder related to early life stress in rodents, primates and humans. So far, no transgenic animal model has been established to validate these findings on a behavioral level. In the present study, we examined the effects of a Morc1 loss of function mutation in female C57BL/6N mice on behavioral correlates of mood disorders like the Forced Swim Test, the Learned Helplessness Paradigm, O-Maze and Dark-Light-Box. We could show that Morc1(-/-) mice display increased depressive-like behavior whereas no behavioral abnormalities regarding locomotor activity or anxiety-like behavior were detectable. CORT plasma levels did not differ significantly between Morc1(-/-) mice and their wildtype littermates, yet - surprisingly - total Bdnf mRNA-levels in the hippocampus were up-regulated in Morc1(-/-) animals. Although further work would be clarifying, Morc1(-/-) mice seem to be a promising epigenetically validated mouse model for depression associated with early life stress.

Keywords: Bdnf; Depression; Early life stress; Epigenetics; Morc1; Transgenic mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Behavior, Animal / physiology*
  • Brain-Derived Neurotrophic Factor / metabolism*
  • Depression / genetics*
  • Disease Models, Animal
  • Epigenesis, Genetic
  • Female
  • Hippocampus / metabolism*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Nuclear Proteins / genetics
  • Nuclear Proteins / physiology*
  • Phenotype
  • RNA, Messenger / metabolism
  • Up-Regulation

Substances

  • Brain-Derived Neurotrophic Factor
  • Morc1 protein, mouse
  • Nuclear Proteins
  • RNA, Messenger