ABSTRACT
Glucocorticosteroids (GCs) are hormones secreted by the adrenals to co-ordinate the body’s response to a multitude of stressors. This endocrine response can be evoked by physical stressors, such as strenuous exercise, and also psychological stressors, such as the worry caused in response to life events and difficulties. Secretion of GCs serves to mobilize energy from storage sites and divert it primarily to cardiovascular, pulmonary, sensory and muscle tissues-places where the need for oxygen and glucose is urgent in order to respond to the perceived demand for action. To help provide this energy, GCs suppress systems that are not crucial in this perceived emergency, including digestion, growth, reproduction and immunity. Although these physiological responses are essential for responding to an acute stressor, the identical responses are also triggered by chronic stressors, and therefore serve as the basis of pathology to the systems involved. When exposure to GCs is prolonged (due to stress, pathologic hypersecretion as in Cushing’s syndrome, or exogenous administration of synthetic GCs such as prednisone, hydrocortisone or dexamethasone), myopathy, fatigue, hypertension, ulcers and increased risk for adult-onset diabetes and neuron death are a few of the noted consequences (Munck et al. 1984). This chapter is concerned with the latter consequence, namely neuron death. The purpose of this chapter is not only to give a short review of the current literature, but also to draw attention to the ramifications of GC effects to neurotoxicology.
