Abstract

The transcription factor c-myb is known to play an important role in the regulation of cellular proliferation and differentiation. Recently, the constitutive and aberrant expression of c-myb in the normal and Cu/Zn SOD mutant mouse brain was reported. However, the expression of c-myb in the process of reactive gliosis is not known yet. Here we report the delayed and protracted induction of c-myb in the brain of mice following kainic acid (KA) induced seizure. Our western blot analysis revealed that the amount of c-myb was dramatically increased in the brain 3 days after KA treatment. The induction of c-myb was sustained for more than 7 days after KA treatment. The c-myb immunoreactivity (IR) was restricted to neurons of the hippocampus in control mice. Three days after KA treatment, a strong c-myb IR was found in reactive astrocytes in the whole areas of the CA3 region. Thereafter, c-myb IR astrocytes were gradually concentrated around the CA3 region undergoing selective neuronal loss. A few c-myb IR astrocytes were continuously persisted in the CA3 region 14 days after KA treatment. These findings suggest a role of c-myb signal pathway in reactive gliosis in mice with KA induced seizure.

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