Mild heat stress induces hormetic effects in protecting the primary culture of mouse prefrontal cerebrocortical neurons from neuropathological alterations.

Hormesis is a dose response phenomenon of cells and organisms to various types of stressors. Mild stress stimulates prosurvival pathways and makes the cells adaptive to stressful conditions. It is a widely used fundamental dose-response phenomenon in many biomedical and toxicological sciences, radiation biology, health science etc. Mild heat stress is an easily applicable hormetic agent that exerts consistent results. In the present investigations mouse cerebrocortical prefrontal neurons from E17 mouse embryos were grown in the laboratory on poly-L-lysine coated glass cover slips. The cells from the mild heat stressed group were subjected to a hyperthermic stress of 38 °C for 30 min every alternate day (i.e. mild heat stress was repeated after 48 h) up to the sixth day. After completion of twenty four hours of the final i.e. third exposure of the mild heat stress, the neurons were fixed for the cytochemical studies of neurofibrillary tangles, senile plaques, lipofuscin granules and Nissl substance. There was highly significant decrease in the neuropathological alterations (viz. deposition of Neurofibrillary tangles, deposition of senile plaques, accumulation of Lipofuscin granules) in the neurons from the mild heat stressed group as compared to control. Moreover, the Nissl substance was significantly preserved in the mild heat stressed group as compared to control. The results indicate that the applied mild heat stress (38 °C for 30 min) exerts beneficial effects on the prefrontal cerebrocortical neurons by slowing down the neuropathological alterations, suggesting the hormetic effect of the mild heat stress.