Chronic stress has been shown to reduce the arbor complexity and total dendritic length of apical dendrite trees of CA3 pyramidal neurons in the hippocampus as well. Chronic stress-induced changes in behavior have usually been attributed to changes in the hippocampus which is a primary neural target of glucocorticoids and is involved in many of the behaviors altered by corticosteroid administration. Both chronic stress and corticosteroid administration result in extensive atrophy of apical dendrites of pyramidal neurons in hippocampal area CA3, and these dendrites do not atrophy when cyanoketone (a corticosteroid blocker) is given. This dendrite atrophy is mediated by both glutaminergic and serotonergic systems (administration of either NMDA receptor antagonist CGP 43487 or serotonin uptake inhibitor tianeptine prevents atrophy). Cell death has been reported to prolonged treatment. Stress hormones in small doses do not themselves cause damage but magnify effects of other dangerous agents, including excitotoxins, hypoglycemia, hypoxia and ischemia. Damaging effects of stress in these neurons are thought to be related to expression of brain-derived neurotrophic factor (BDNF), the expression of which is reduced in stressed conditions and increased with the administration of anti-depressants.