We examined whether ischemia/reperfusion would cause rapid changes in brain levels of heat shock protein 70 (HSP 70) and brain nitric oxide synthase (bNOS) Additional stresses such as seizure activity often occur following recovery from ischemia, and altered production of HSP 70 and bNOS may influence neurological sequelae. Total global ischemia was produced for 5-10 minutes by raising intracranial pressure. After 4 hours of reperfusion, HSP 70 and bNOS were evaluated by western blotting, and data reported as percent increase over time-control samples. HSP 70 increased in the cerebellum and in the hippocampus (187±22%, n = 10 and 87±4%, n = 4, respectively), while no consistent increase was apparent in cerebral cortex. In addition, there were no substantial changes in bNOS at 4 hours In order to assess the location of HSP 70 in the cerebellum, we performed immunohistochemistry on 50 μm frozen sections. Light microscopy revealed widespread HSP 70 immunoreactivity, and pronounced staining of the granule cell layer of the cerebellum. We conclude that alterations in protein synthesis following ischemia are region- and protein-specific.
|Publication status||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology