作者: Hymie Anisman , Zul Merali , John D.H. Stead
DOI: 10.1016/J.NEUBIOREV.2008.03.001
关键词: Anxiety 、 Sensitization 、 Corticotropin-releasing hormone 、 Neurochemical 、 Animal studies 、 Anxiety disorder 、 Neuroscience 、 Psychology 、 Endocrinology 、 Epigenetics 、 Stressor 、 Internal medicine
摘要: Stressful events have been implicated in the precipitation of depression and anxiety. These disorders may evolve owing to one or more an array neuronal changes that occur several brain regions. It seems likely these stressor-provoked neurochemical alterations are moderated by genetic determinants, as well a constellation experiential environmental factors. Indeed, animal studies shown vulnerability depressive-like behaviors involve mechanisms similar those associated with human (e.g., altered serotonin, corticotropin releasing hormone their receptors, growth factors), effects stressors influenced previous stressor experiences, particularly encountered early life. might reflect sensitization functioning, phenotypic processes lead release receptor sensitivity, epigenetic modify expression specific genes reactivity. is suggested life-long disorder, which even after effective treatment, has high rate re-occurrence sensitized factors promote persistent gene expression.