Figure 2.

Summary of the delayed effects of stress on hippocampal neurons and astrocytes, reflecting primarily genomically-mediated effects of GCs. Over the course of minutes to hours after a stressor exposure, GCs increase AMPAR and NMDAR insertion into the post-synaptic membrane but reduce plasma membrane GluTs. Glucose transport and metabolism are downregulated in astrocytes and neurons, production and metabolism of lactate is lowered, and expression of prometabolic genes is reduced. The overall effect, under normal physiological circumstances, is to downregulate both neuronal firing and metabolism, acting to reverse the short-term impact of stress and promote optimal memory for stress-related events with minimal or no cellular damage. The increase in glutamate receptors may potentiate the response to subsequent or prolonged stress, potentially including excitotoxic damage.