Kasper Siegfried, McEwen Bruce S
Department of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria.
CNS Drugs. 2008;22(1):15-26. doi: 10.2165/00023210-200822010-00002.
The precise neurobiological processes involved in depression are not clear, but it is recognized that numerous factors are involved, including changes in neurotransmitter systems and brain plasticity. Neuroplasticity refers to the ability of the brain to adapt functionally and structurally to stimuli. Impairment of neuroplasticity in the hippocampus, amygdala and cortex is hypothesized to be the mechanism by which cognitive function, learning, memory and emotions are altered in depression. The mechanisms underlying alterations in neuroplasticity are believed to relate to changes in neurotransmitters, hormones and growth factors. Structural changes in the hippocampus that have been proposed to be associated with depression include dendritic atrophy, reduced levels of cerebral metabolites, decreased adult neurogenesis (generation of new nerve cells) and reduced volume. Increased dendritic branching occurs in the basolateral nucleus of the amygdala. Reduced neuronal size and glial cell density occur in the prefrontal cortex. Clinically, tianeptine is an antidepressant effective in reducing symptoms of depression in mild to moderate-to-severe major depression, including over the long term. Tianeptine is also effective in alleviating the symptoms of depression-associated anxiety. It is generally well tolerated, with little sedation or cognitive impairment. The efficacy profile of tianeptine could be explained by its neurobiological properties observed in animal models. Tianeptine prevents or reverses stress-associated structural and cellular changes in the brain and normalizes disrupted glutamatergic neurotransmission. In particular, in the hippocampus, it prevents stress-induced dendritic atrophy, improves neurogenesis, reduces apoptosis and normalizes metabolite levels and hippocampal volume. Tianeptine also has beneficial effects in the amygdala and cortex and can reverse the effects of stress on neuronal and synaptic functioning. The neurobiological properties of tianeptine may provide an explanation not only for its antidepressant activity, but also for its anxiolytic effects in depressed patients and its lack of adverse effects on cognitive function and memory.
抑郁症所涉及的确切神经生物学过程尚不清楚,但人们认识到有许多因素参与其中,包括神经递质系统的变化和大脑可塑性。神经可塑性是指大脑在功能和结构上适应刺激的能力。海马体、杏仁核和皮质的神经可塑性受损被认为是抑郁症中认知功能、学习、记忆和情绪发生改变的机制。神经可塑性改变的潜在机制被认为与神经递质、激素和生长因子的变化有关。已提出的与抑郁症相关的海马体结构变化包括树突萎缩、脑代谢物水平降低、成年神经发生减少(新神经细胞的产生)和体积减小。杏仁核基底外侧核出现树突分支增加。前额叶皮质出现神经元大小减小和胶质细胞密度降低。临床上,噻奈普汀是一种抗抑郁药,对减轻轻度至中度至重度重度抑郁症的症状有效,包括长期有效。噻奈普汀还能有效缓解与抑郁症相关的焦虑症状。它通常耐受性良好,几乎没有镇静作用或认知损害。噻奈普汀的疗效可以用在动物模型中观察到的神经生物学特性来解释。噻奈普汀可预防或逆转大脑中与压力相关的结构和细胞变化,并使被破坏的谷氨酸能神经传递正常化。特别是在海马体中,它可预防压力诱导的树突萎缩,改善神经发生,减少细胞凋亡,并使代谢物水平和海马体体积正常化。噻奈普汀在杏仁核和皮质中也有有益作用,并可逆转压力对神经元和突触功能的影响。噻奈普汀的神经生物学特性不仅可以解释其抗抑郁活性,还可以解释其对抑郁症患者的抗焦虑作用以及对认知功能和记忆无不良反应的原因。