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Heat shock response in the central nervous system
1Neurology and Medical Service, Massachusetts General Hospital, Harvard Medical School, Boston.
Experientia
|November 30, 1994
Summary
The heat shock response protects nervous tissue from injury by reducing excitotoxicity. Protein synthesis is essential for this neuroprotective effect, offering potential therapeutic strategies for brain injury.
Area of Science:
- Neuroscience
- Cellular Biology
- Biochemistry
Background:
- The heat shock response (HSR) is activated in nervous tissue under various stress conditions, including ischemic brain injury, trauma, and seizures.
- Excitotoxicity, driven by excessive excitatory neurotransmission, contributes to neuronal death in similar pathophysiological states.
Purpose of the Study:
- To investigate whether pre-induction of the heat shock response can protect against glutamate-induced excitotoxicity in vitro.
- To determine the role of protein synthesis in mediating heat shock-induced neuroprotection.
Main Methods:
- Induction of the heat shock response via short thermal stress in vitro.
- Assessment of glutamate-induced excitotoxicity.
- Analysis of protein synthesis and heat shock protein (HSP) mRNA expression.
Main Results:
- Prior induction of the heat shock response significantly attenuated glutamate-induced excitotoxicity in vitro.
- Thermal stress triggered characteristic HSR protein synthesis and increased HSP mRNA expression.
- Inhibition of protein synthesis abolished the neuroprotective effect of the heat shock response.
Conclusions:
- The heat shock response confers neuroprotection against excitotoxicity, mediated by induced protein synthesis.
- Understanding HSP mechanisms may reveal targets for treating excitotoxic neuronal injury.
- In vivo studies suggest thermal or ischemic preconditioning offers protection against subsequent insults.