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慢性应激诱导外侧杏仁核谷氨酸能神经元损伤的机制。

Mechanism of Chronic Stress-Induced Glutamatergic Neuronal Damage in the Basolateral Amygdaloid Nucleus.

机构信息

Hebei Key Laboratory of Forensic Medicine, Collaborative Innovation Center of Forensic Medical Molecular Identification, Department of Forensic Medicine, Hebei Medical University, Shijiazhuang, China.

出版信息

Anal Cell Pathol (Amst). 2021 Nov 23;2021:8388527. doi: 10.1155/2021/8388527. eCollection 2021.

Abstract

Stress is a ubiquitous part of our life, while appropriate stress levels can help improve the body's adaptability to the environment. However, sustained and excessive levels of stress can lead to the occurrence of multiple devastating diseases. As an emotional center, the amygdala plays a key role in the regulation of stress-induced psycho-behavioral disorders. The structural changes in the amygdala have been shown to affect its functional characteristics. The amygdala-related neurotransmitter imbalance is closely related to psychobehavioral abnormalities. However, the mechanism of structural and functional changes of glutamatergic neurons in the amygdala induced by stress has not been fully elucidated. Here, we identified that chronic stress could lead to the degeneration and death of glutamatergic neurons in the lateral amygdaloid nucleus, resulting in neuroendocrine and psychobehavioral disorders. Therefore, our studies further suggest that the Protein Kinase R-like ER Kinase (PERK) pathway may be therapeutically targeted as one of the key mechanisms of stress-induced glutamatergic neuronal degeneration and death in the amygdala.

摘要

压力是我们生活中无处不在的一部分,而适当的压力水平可以帮助提高身体对环境的适应能力。然而,持续和过高的压力水平会导致多种毁灭性疾病的发生。作为情绪中心,杏仁核在调节应激诱导的心理行为障碍方面起着关键作用。杏仁核的结构变化已被证明会影响其功能特征。杏仁核相关神经递质失衡与心理行为异常密切相关。然而,应激诱导的杏仁核谷氨酸能神经元的结构和功能变化的机制尚未完全阐明。在这里,我们发现慢性应激可导致外侧杏仁核谷氨酸能神经元的退化和死亡,导致神经内分泌和心理行为障碍。因此,我们的研究进一步表明,蛋白激酶 R 样内质网激酶(PERK)途径可能是一种有治疗潜力的靶点,作为应激诱导的杏仁核谷氨酸能神经元退化和死亡的关键机制之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa06/8632434/0e4201523e82/ACP2021-8388527.001.jpg

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