We can all relate to the side effects of severe stress in one way or the other. Severe stress affects us in many ways and contributes immensely to many pathological issues. One side effect of stress is spatial memory impairment.
Whereas non-epigenetic basis of how stress impacts our spatial memory has been documented, no such work has been done to determine the epigenetic basis of stress-related spatial memory impairment. Armed with the fact that spatial training and intense stress exhibit opposing effects on histone acetylation balance, a team of Colombian scientists hypothesized that histone acetylation balance disruption may be the culprit behind stress-induced spatial memory lapses and that inactivating the histone deacetylase enzyme may prevent such lapses.
To achieve their aim, the team led by Alejandro Munera trained male Wistar rats in spatial tasks in the Barnes maze with 1-h movement restraint imposed on half of the rats before training. After the training, stressed and non-stressed rats were randomly selected to either receive 1 mg/kg of TSA or a vehicle peritoneally. 24-hr later the team tested long-term spatial memory in all the rats. After the test, the team also collected plasma and brain tissue in order to measure corticosterone levels and histone H3 acetylation in several areas of the brain.
Here is what they found:
- Stressed animals that received the vehicle showed memory impairment, increased plasma, corticosterone levels, and significant reduction in histone H3 acetylation in the prelimbic cortex and hippocampus areas of the brain.
- However, stressed animals that received the histone deacetylase inhibitor TSA did not show such effects.
To learn more about this important masterpiece orient your way to Neurobiology, August 2016.