INTRODUCTION
Stress and Depression
Depressive disorders are widely regarded as stress-related conditions. Although genetic vulnerability is critical to the development of depression, in the absence of environmental stressors, the incidence of depressive disorders is very low (Kendler et al., 1995), and in approximately 75% of cases of depression there is a precipitating life event (Brown & Harris, 1978; Frank, Anderson, Reynolds, Ritenour, & Kupfer, 1994). Living organisms survive by maintaining a complex dynamic equilibrium or homeostasis that is constantly challenged by intrinsic or extrinsic stressors. These stressors set in motion responses aimed at preserving homeostasis, including activation of a wide variety of neurotransmitters and neuromodulators. The hypothalamic pituitary adrenal (HPA) axis is the body's main stress hormonal system. Corticotropin releasing hormone (CRH) is the principal central effector of the stress response (Chrousos & Gold, 1992). CRH triggers the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary corticotrope, which, in turn, triggers the release of adrenal glucocorticoids. The stress response is terminated by glucocorticoid feedback at brain and pituitary sites.
Depression has been conceptualized as maladaptive, exaggerated responses to stress. Abnormalities of the HPA axis, as manifested by hypercortisolemia and disruption of the circadian rhythm of cortisol secretion, are well established phenomena in depression (Carroll, Curtis, & Mendels, 1976; Sachar et al., 1973).