Gγ7-specific prothymosin alpha deletion causes stress- and age-dependent motor dysfunction and anxiety

Biochem Biophys Res Commun. 2020 Jan 29;522(1):264-269. doi: 10.1016/j.bbrc.2019.11.103. Epub 2019 Nov 20.

Abstract

We previously showed that prothymosin alpha (ProTα) improves cerebral ischemia-induced motor dysfunction. Our recent study also demonstrated that heterozygous ProTα deletion exhibited an enhanced anxiety-like behavior in mice. However, it remains elusive which brain regions or cells are related to these phenotypes. Here we generated conditional Gγ7-specific ProTα knockout mice using G protein γ7 subunit gene (Gng7)-cre promoter to see the brain robustness roles of ProTα in the striatum and hippocampus. The younger conditional ProTα (Gng7) knockout mice at the age of 10 weeks showed no significant phenotypes in motor dysfunction in the Rotarod test and locomotor activity in the open-field test, whereas significant motor dysfunction was obtained by 15 min transient middle cerebral artery occlusion (tMCAO)-induced cerebral ischemia. The aged conditional ProTα (Gng7) knockout mice at the age of 20 weeks showed hypolocomotor activity with less center time in the open-field test and impaired motor coordination in the Rotarod test without ischemia. Thus, this study suggests that ProTα has important roles in the maintenance of motor coordination and anxiety-like behavior.

Keywords: Cerebral ischemia; Locomotor activity; Motor coordination; Prothymosin alpha.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging
  • Animals
  • Anxiety / genetics*
  • Anxiety / physiopathology
  • Brain Ischemia / genetics
  • Brain Ischemia / physiopathology
  • Female
  • GTP-Binding Protein gamma Subunits / genetics*
  • Gene Deletion
  • Locomotion*
  • Male
  • Mice
  • Mice, Knockout
  • Protein Precursors / genetics*
  • Psychomotor Performance
  • Thymosin / analogs & derivatives*
  • Thymosin / genetics

Substances

  • GTP-Binding Protein gamma Subunits
  • Gng7 protein, mouse
  • Protein Precursors
  • prothymosin alpha
  • Thymosin