Loss of GSK-3 Causes Abnormal Astrogenesis and Behavior in Mice

Eui Man Jung, Minhan Ka, Woo Yang Kim

Research output: Contribution to journalArticlepeer-review

30 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)3954-3966
Number of pages13
JournalMolecular Neurobiology
Issue number6
StatePublished - Aug 1 2016


  • Astrocyte
  • Astrogenesis
  • Brain size
  • GFAP
  • GSK-3
  • Hypertrophy

ASJC Scopus subject areas

  • Neurology
  • Cellular and Molecular Neuroscience


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