| First Author | Halder SK | Year | 2020 |
| Journal | Biochem Biophys Res Commun | Volume | 522 |
| Issue | 1 | Pages | 264-269 |
| PubMed ID | 31759625 | Mgi Jnum | J:291693 |
| Mgi Id | MGI:6445402 | Doi | 10.1016/j.bbrc.2019.11.103 |
| Citation | Halder SK, et al. (2020) Ggamma7-specific prothymosin alpha deletion causes stress- and age-dependent motor dysfunction and anxiety. Biochem Biophys Res Commun 522(1):264-269 |
| abstractText | We previously showed that prothymosin alpha (ProTalpha) improves cerebral ischemia-induced motor dysfunction. Our recent study also demonstrated that heterozygous ProTalpha 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 Ggamma7-specific ProTalpha knockout mice using G protein gamma7 subunit gene (Gng7)-cre promoter to see the brain robustness roles of ProTalpha in the striatum and hippocampus. The younger conditional ProTalpha (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 ProTalpha (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 ProTalpha has important roles in the maintenance of motor coordination and anxiety-like behavior. |
