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{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/3649690","sourcedb":"PMC","sourceid":"3649690","source_url":"http://www.ncbi.nlm.nih.gov/pmc/3649690","text":"8. Stress, Depression, and Reduced Neural Plasticity\nThe hippocampal formation is an area rich in mineralocorticoid (MRs) and glucocorticoid receptors (GRs). These receptors function in the maintenance of basal HPA tone and in the regulation of negative feedback of glucocorticoid release during a stress response [68]. Given this, it is not surprising that the hippocampus is particularly vulnerable to the effects of stress and depression [69, 70]. Depressed patients have reduced hippocampal volume which varies with the number of episodes and duration of the illness [71–73]. Similarly, postmortem studies of hippocampal tissue collected from depressed patients have shown alterations in gray matter density, reductions in neuropil, and decreased hippocampal neurogenesis [22, 23, 74–77]. Animal models of depression using exposure to chronic stress demonstrate the same changes in hippocampal structure and show reductions in neural plasticity, including reductions in neurogenesis and the expression of proteins associated with neural plasticity [21, 64, 65, 78]. Chronic stress exposure also reduces dendrite length and complexity [79, 80], spine density [81], and NCAM expression [65] and modifies expression of synaptic SNARE proteins [82] in the hippocampus. \nStabilization of the HPA axis by antidepressants is associated with improved mood scores that either precedes or is coincident with the behavioural alleviation of depressive symptoms in humans [61]. Thus the improvements in negative feedback inhibition of the HPA axis that correspond to improvement in depressive symptoms with antidepressant treatment may be attributable to neural adaptation in limbic structures that regulate feedback inhibition of HPA axis such as the hippocampus. Interestingly chronic antidepressant treatment is seen to reverse the negative effects of stress on hippocampal volume [65, 83], though the exact contribution of neural plastic elements that underlie this enhancement is not fully 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