Glucocorticoids, metabolism and brain activity

The review integrates different experimental approaches including biochemistry, c-Fos expression, microdialysis (glutamate, GABA, noradrenaline and serotonin), electrophysiology and fMRI to better understand the effect of elevated level of glucocorticoids on the brain activity and metabolism. The available data indicate that glucocorticoids alter the dynamics of neuronal activity leading to context-specific changes including both excitation and inhibition and these effects are expected to support the task-related responses. Glucocorticoids also lead to diversification of available sources of energy due to elevated levels of glucose, lactate, pyruvate, mannose and hydroxybutyrate (ketone bodies), which can be used to fuel brain, and facilitate storage and utilization of brain carbohydrate reserves formed by glycogen. However, the mismatch between carbohydrate supply and utilization that is most likely to occur in situations not requiring energy-consuming activities lead to metabolic stress due to elevated brain levels of glucose. Excessive doses of glucocorticoids also impair the production of energy (ATP) and mitochondrial oxidation. Therefore, glucocorticoids have both adaptive and maladaptive effects consistently with the concept of allostatic load and overload.

Automated summary

The review integrates various experimental approaches to better understand the effects of elevated glucocorticoids on brain activity and metabolism. It suggests that glucocorticoids alter neuronal activity dynamics, leading to context-specific changes in both excitation and inhibition, which support task-related responses. Glucocorticoids also diversify energy sources for the brain and impact carbohydrate reserves, with potential stress due to mismatches in supply and utilization.