Neuroendocrinology of Stress

Abstract:

The response to stress involves the active release of hormones and other mediators that produce adaptation in the aftermath of acute stress (allostasis) and yet can lead to pathophysiology when the same mediators are not shut off or are dysregulated over weeks and months (allostatic load). The brain is the key organ of stress since it interprets what is potentially threatening and therefore stressful and it determines the behavioral and physiological responses of the individual. Behavioral responses include fighting or fleeing, eating too much of the wrong things, smoking, drinking and losing sleep at night. Behavioral responses may also include health promoting behaviors such as regular moderate exercise. Hence lifestyle and behavior are key contributors or “being stressed out” and hence to allostatic load. The brain also is a target of stress and remodeling of dendrites and formation or down-regulation of synapses is a key aspect. In hippocampus and prefrontal cortex, repeated stress causes dendrites to shrink and spine synapses to decrease in number whereas in basolateral amygdala stress causes increased dendritic branching and synapse density. Mediators of structural remodeling include not only adrenal steroids but endogenous neurotransmitters, neurotrophins, the extracellular protease, tissue plasminogen activator, and cell surface adhesion molecules. Remodeling of neural circuitry under repeated stress leads to impaired memory, increased anxiety and aggression and impaired attention. Changes of this type may occur in depression and anxiety disorders.