Reduction in heat shock protein 90 correlates to neuronal vulnerability in the rat piriform cortex following status epilepticus

- HSP70 was increased in CA3 pyramidal cells and dentate granule cells following SE.
- HSP90 was decreased in CA1-3 pyramidal cells after SE.
- HSP70 was transiently increased in PC neurons following SE.
- HSP90 was decreased in PC neurons after SE.
- HSP90 degradation may be closely related to neuronal vulnerability to SE insult.

In the present study, we addressed the question of whether the distinct patterns of heat shock protein (HSP) 70 and HSP90 expressions in the brain region represents the regional specific responses to status epilepsticus (SE) in an effort to better understand the role of HSPs in epileptogenic insult. HSP70 immunoreactivity was increased in CA3 pyramidal cells as well as dentate granule cells at 12 h-1 week after SE. HSP70 immunoreactivity was transiently increased in neurons within the piriform cortex (PC) following SE. Linear regression analysis showed no correlation between the intensity of NeuN and that of HSP70. In contrast to HSP70, HSP90 immunoreactivity was decreased in CA1-3 pyramidal cells at 4 days-4 weeks after SE. In addition, HSP90 immunoreactivity was decreased in PC neurons at 12 h-4 weeks after SE. linear regression analysis showed a direct proportional relationship between the intensity of NeuN and that of HSP90. Therefore, these findings suggest that HSP90 degradation may be closely related to neuronal vulnerability to SE insult.