Abstract
Increasing evidence demonstrates a connection between growth factor function (including brain-derived neurotrophic factor, BDNF), glucocorticoid levels (one of the steroid hormones), and the pathophysiology of depressive disorders. Because both BDNF and glucocorticoids regulate synaptic function in the central nervous system, their functional interaction is of major concern. Interestingly, alterations in levels of estrogen, another steroid hormone, may play a role in depressive-like behavior in postpartum females with fluctuations of BDNF-related molecules in the brain. BDNF and cytokines, which are protein regulators of inflammation, stimulate multiple intracellular signaling cascades involved in neuropsychiatric illness. Pro-inflammatory cytokines may increase vulnerability to depressive symptoms, such as the increased risk observed in patients with cancer and/or autoimmune diseases. In this review, we discuss the possible relationship between inflammation and depression, in addition to the cross-talk among cytokines, BDNF, and steroids. Further, since nutritional status has been shown to affect critical pathways involved in depression through both BDNF function and the monoamine system, we also review current evidence surrounding diet and supplementation (e.g., flavonoids) on BDNF-mediated brain functions.
Highlights
In addition to genetic pre-dispositions, various environmental factors are well-established to contribute to the pathogenesis of depressive disorders
Ample evidence demonstrates that glucocorticoid levels regulate neuronal transmission and synaptic plasticity [2], though abnormally elevated levels are recognized as a risk for depressive disorders [3]
It is possible that amygdala ERα plays a role in depressive-like behaviors, and that the brain-derived neurotrophic factor (BDNF)/TrkB/extracellular signal-regulated kinase (ERK) system functions to recover from postpartum depression (PPD), further study is required to reveal a relationship between function of ERα and upregulation of BDNF in our model
Summary
In addition to genetic pre-dispositions, various environmental factors are well-established to contribute to the pathogenesis of depressive disorders. It has been reported that postpartum rats after chronic stress during their pregnant period exhibit depressive-like behavior, impaired ability to care for their young, and decreased spine density of pyramidal neurons in the medial prefrontal cortex [41]. Administration of 17β estradiol and propyl pyrazole-triol (PPT, selective ERα agonist) in primiparous mothers caused significant upregulation of BDNF, TrkB, and pERK2 in the medial amygdala, in addition to marked improvement of depressive-like behaviors [Ref.
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