Induction of transcription factor A-myb expression in reactive astrocytes following an excitotoxic lesion in the mouse hippocampus

Neurochem Res. 2006 Nov;31(11):1371-4. doi: 10.1007/s11064-006-9184-x. Epub 2006 Oct 20.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / drug effects
  • Astrocytes / metabolism*
  • Blotting, Western
  • Densitometry
  • Excitatory Amino Acid Agonists / administration & dosage
  • Excitatory Amino Acid Agonists / toxicity*
  • Fluorescent Antibody Technique
  • Hippocampus / pathology*
  • Immunohistochemistry
  • Injections, Intraventricular
  • Kainic Acid / administration & dosage
  • Kainic Acid / toxicity*
  • Male
  • Mice
  • Mice, Inbred ICR
  • Proto-Oncogene Proteins / biosynthesis*
  • Proto-Oncogene Proteins c-myb
  • Signal Transduction / drug effects
  • Trans-Activators / biosynthesis*

Substances

  • Excitatory Amino Acid Agonists
  • Mybl1 protein, mouse
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-myb
  • Trans-Activators
  • Kainic Acid