| First Author | Jung EM | Year | 2016 |
| Journal | Mol Neurobiol | Volume | 53 |
| Issue | 6 | Pages | 3954-3966 |
| PubMed ID | 26179612 | Mgi Jnum | J:311069 |
| Mgi Id | MGI:6765065 | Doi | 10.1007/s12035-015-9326-8 |
| Citation | Jung EM, et al. (2016) Loss of GSK-3 Causes Abnormal Astrogenesis and Behavior in Mice. Mol Neurobiol 53(6):3954-3966 |
| abstractText | Altered activity of glycogen synthase kinase-3 (GSK-3) is associated with psychiatric diseases and neurodegenerative diseases. GSK-3 is a key regulator in multiple aspects of neuronal differentiation in the brain. However, little is known about the role of GSK-3 in astrocyte development. To examine the role of GSK-3 in astrocytes, we generated a conditional knockout mouse using a glial fibrillary acidic protein (GFAP)-cre driver, in which the GSK-3 alpha and beta genes are deleted in astrocytes. We found that GFAP-cre-mediated GSK-3 deletion led to a larger brain. The number and size of astrocytes were increased in GSK-3 mutant brains. The levels of GFAP and phospho-STAT3, indicators of astrogenesis, were elevated in GSK-3 mutants. Furthermore, we found upregulation of astrocyte regulatory molecules such as phospho-AKT, phospho-S6, and cyclin D in GSK-3 mutant brains. Finally, GSK-3 mutant mice exhibited aberrant anxiety and social behavior. Our results suggest that GSK-3 plays a significant role in astrocyte development and behavioral control in mice. |
