Effects of heat environments on depressive disorders: Neurogenesis-mediated mechanisms

Heat may induce depressive disorders by affecting hippocampal neurogenesis. Heat stress may activate the hypothalamic-pituitary-adrenal (HPA) axis, leading to elevated glucocorticoid levels, which in turn cause hippocampal damage, suppress the expression of brain-derived neurotrophic factor (BDNF), impair neurogenesis and synaptic plasticity, and ultimately promote the onset of depression. Glucocorticoid receptors play a dual regulatory role in this process: moderate upregulation can counteract stress, but their deficiency or overactivation may impair both the BDNF signaling pathway and the negative feedback regulation of the HPA axis. Prolonged heat exposure may lead to overexpression of heat shock proteins, resulting in neurotoxicity, and by promoting excessive activation of glucocorticoid receptors, further exacerbating damage to the BDNF-TrkB-PI3K/AKT signaling pathway. In terms of treatment, antidepressant medications and some nonpharmacological interventions can increase BDNF levels and partially reverse defects in neurogenesis. The effects of moderate heat training on BDNF levels and improvements in depression require further study.