Abstract:

Activation of the hypothalamic-pituitary-adrenal (HPA) axis and alterations of the neuronal plasticity are hypothesized to be the etiology underlying depressive disorders. Glucocorticoid receptor (GR), as an important part of the HPA axis negative feedback circuit, regulates the responses of HPA axis to stress stimuli. The dysfunction of the GR induces the hyperactivity of the HPA axis and excessive glucocorticoid production, which lead to damages in neuronal plasticities and finally result in depression. The function of GR is regulated by its single nucleotide polymorphisms and the molecular chaperones. This review will focus on the possible mechanisms of GR dysfunction caused by the single nucleotide polymorphisms of GR gene and the alterations of molecular chaperones.

Key words: depression, glucocorticoid receptor, single nucleotide polymorphism, molecular chaperones