Tarai Shashikanta, Mukherjee Rupsha, Gupta Sharda, Rizvanov Albert A, Palotás Andras, Chandrasekhar Pammi V S, Bit Arindam
2Department of Humanities and Social Science, National Institute of Technology, Raipur, India.
1Department of Biomedical Engineering, National Institute of Technology, Raipur, India.
Cogn Neurodyn. 2019 Jun;13(3):219-237. doi: 10.1007/s11571-019-09522-3. Epub 2019 Feb 1.
Stress-induced major depression and mood disorders are characterized by behavioural abnormalities and psychiatric illness, leading to disability and immature mortality worldwide. Neurobiological mechanisms of stress and mood disorders are discussed considering recent findings, and challenges to enhance pharmacological effects of antidepressant, and mood stabilizers. Pharmacological enhancement of ketamine and scopolamine regulates depression at the molecular level, increasing synaptic plasticity in prefrontal regions. Blood-derived neurotrophic factors facilitate mood-deficit symptoms. Epigenetic factors maintain stress-resilience in hippocampal region. Regulation of neurotrophic factors blockades stress, and enhances neuronal survival though it paralyzes limbic regions. Molecular agents and neurotrophic factors also control behavioral and synaptic plasticity in addiction and stress disorders. Future research on neuronal dynamics and cellular actions can be directed to obtain the etiology of synaptic dysregulation in mood disorder and stress. For the first time, the current review contributes to the literature of synaptic plasticity representing the role of epigenetic mechanisms and glucocorticoid receptors to predict depression and anxiety in clinical conditions.
应激诱导的重度抑郁症和情绪障碍的特征是行为异常和精神疾病,在全球范围内导致残疾和过早死亡。结合最近的研究结果,讨论了应激和情绪障碍的神经生物学机制,以及增强抗抑郁药和情绪稳定剂药理作用所面临的挑战。氯胺酮和东莨菪碱的药理增强作用在分子水平上调节抑郁,增加前额叶区域的突触可塑性。血液源性神经营养因子会加重情绪缺陷症状。表观遗传因素维持海马区的应激恢复能力。神经营养因子的调节可阻断应激,并通过麻痹边缘区域来提高神经元存活率。分子药物和神经营养因子也控制成瘾和应激障碍中的行为和突触可塑性。未来关于神经元动力学和细胞作用的研究可以针对情绪障碍和应激中突触失调的病因。本综述首次为代表表观遗传机制和糖皮质激素受体作用的突触可塑性文献做出贡献,以预测临床情况下的抑郁和焦虑。