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Cortical spreading depression increases protein synthesis and upregulates basic fibroblast growth factor
N Kawahara1, C A Ruetzler, G Mies
1Stroke Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892, USA. kawahara-tky@umin.ac.jp
Experimental Neurology
|August 17, 1999
Summary
Cortical spreading depression (CSD) triggers neuroprotection against ischemic damage. This protective effect involves increased trophic factors and glial cell activation, not reduced energy metabolism, offering long-lasting brain protection.
Area of Science:
- Neuroscience
- Cerebrovascular Research
- Cellular Biology
Background:
- Cortical spreading depression (CSD) is known to confer neuroprotection against ischemic injury.
- Previous studies demonstrated protective effects when CSD was induced 24 hours or 3 days before ischemia.
Purpose of the Study:
- To investigate the underlying mechanisms of neuroprotection induced by CSD.
- To differentiate the effects of CSD induction from general cortical stimulation.
Main Methods:
- Induction of repetitive CSD waves in Sprague-Dawley rats using topical KCl application.
- Measurement of cerebral glucose utilization and protein synthesis in cortical and subcortical regions.
- Immunohistochemical analysis of glial fibrillary acidic protein (GFAP) and basic fibroblast growth factor (bFGF).
Main Results:
- CSD induction (KCl group) led to increased cortical and hippocampal protein synthesis.
- Both KCl and NaCl groups showed reduced cerebral glucose utilization.
- CSD group exhibited rapid activation of reactive astrocytes and increased bFGF levels compared to the NaCl group.
Conclusions:
- CSD-induced ischemic tolerance is not mediated by reduced energy metabolism.
- Neuroprotection is associated with the upregulation of trophic factors and glial cell activation.
- These changes suggest a mechanism for long-lasting neuroprotection following CSD.