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Fluorescence Activated Cell Sorting (FACS) and Gene Expression Analysis of Fos-expressing Neurons from Fresh and Frozen Rat Brain Tissue
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Neuronal NOS inhibitor that reduces oxidative DNA lesions and neuronal sensitivity increases the expression of intact

J Cui1, P K Liu

  • 1Department of Neurosurgery, Baylor College of Medicine, Houston, Tex 77030, USA.

Journal of Biomedical Science
|July 17, 2001
PubMed

Insights

Oxidative stress in ischemic brains increases c-fos gene expression. Inhibiting nitric oxide reduces gene damage and neuronal sensitivity, suggesting its role in brain injury mechanisms.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Ischemic brain injury triggers immediate early gene induction due to nuclear gene damage from oxidative stress.
  • Antioxidants mitigate gene damage and subsequent cell death, highlighting the role of oxidative processes.

Purpose of the Study:

  • To investigate the transcriptional mechanism of neuronal sensitivity following ischemia-reperfusion brain injury.
  • To examine the role of nitric oxide in c-fos gene transcription and neuronal response to brain injury.

Main Methods:

  • Utilized focal cerebral ischemia-reperfusion in Long-Evans hooded rats.
  • Quantified c-fos mRNA expression using RNase A protection assay (RPA).
  • Administered 3-bromo-7-nitroindazole to assess nitric oxide's effect.

Main Results:

  • Observed a significant increase in c-fos mRNA in the ischemic cortex immediately post-injury (p < 0.01).
  • c-fos transcript sensitivity to RPA changed upon reperfusion.
  • Injection of 3-bromo-7-nitroindazole (25 mg/kg) significantly increased RPA resistance (42%, p < 0.03), indicating reduced gene damage and neuronal sensitivity.

Conclusions:

  • Neuronal nitric oxide synthase activity is linked to neuronal sensitivity during ischemia-reperfusion.
  • Aberrant mRNA transcripts from genes with oxidative damage may contribute to neuronal sensitivity in ischemic brain injury.

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