Neurochemical Research

, Volume 31, Issue 11, pp 1371–1374

Induction of Transcription Factor A-myb Expression in Reactive Astrocytes Following an Excitotoxic Lesion in the Mouse Hippocampus

Authors

  • Gye Sun Jeon
    • Department of AnatomySeoul National University College of Medicine
  • Hee Jine Byun
    • Department of AnatomySeoul National University College of Medicine
  • Sung Kyung Park
    • Department of AnatomySeoul National University College of Medicine
  • Sang Wook Park
    • Department of AnatomySeoul National University College of Medicine
  • Dong Woon Kim
    • Department of AnatomySeoul National University College of Medicine
  • Je Hoon Seo
    • Department of AnatomyChungbuk National University College of Medicine
  • Choong Ik Cha
    • Department of AnatomySeoul National University College of Medicine
    • MRC Neuroscience Research InstituteSeoul National University College of Medicine
    • Department of AnatomySeoul National University College of Medicine
    • MRC Neuroscience Research InstituteSeoul National University College of Medicine
Original Paper

DOI: 10.1007/s11064-006-9184-x

Cite this article as:
Jeon, G.S., Byun, H.J., Park, S.K. et al. Neurochem Res (2006) 31: 1371. doi:10.1007/s11064-006-9184-x

Abstract

In the present study, we examined patterns of A-myb expression in the kainic acid (KA)-treated mouse hippocampus. Western blot analysis revealed that A-myb expression was dramatically increased in brain 3 days after KA treatment, and was sustained for more than 7 days. A-myb immunoreactivity was restricted to hippocampal neurons in control mice. Three days after KA treatment, strong A-myb immunoreactivity was observed in reactive astrocytes throughout the CA3 region. Thereafter, A-myb immunoreactive astrocytes gradually concentrated around the CA3 region in parallel with selective neuronal loss, and only a few A-myb immunoreactive astrocytes persisted in the CA3 region 14 days after KA treatment. These findings suggest that the A-myb plays a role in the reactive gliosis signaling pathway in KA-induced excitotoxic lesions.

Keywords

A-mybReactive astrocytesKainic acidHippocampus

Copyright information

© Springer Science+Business Media, LLC 2006