Neural plasticity to stress and antidepressant treatment

摘要: Adaptations at the cellular and molecular levels in response to stress antidepressant treatment could represent a form of neural plasticity that contributes pathophysiology depression. At level, atrophy death stress-vulnerable neurons hippocampus, as well decreased neurogenesis hippocampal neurons, has been reported preclinical studies. Clinical studies also provide evidence for cell prefrontal cortex. It is possible oppose these adverse effects, which may be regarded loss plasticity, by blocking or reversing increasing survival function. The mechanisms underlying effects are discussed, including role cAMP signal transduction cascade neurotrophic factors.