Department of Neuroscience, The Ohio State University, Columbus, OH 43210, USA.
Center for Brain and Spinal Cord Repair, The Ohio State University, Columbus, OH 43210, USA.
Neural Plast. 2017;2017:8640970. doi: 10.1155/2017/8640970. Epub 2017 Aug 8.
Stress, injury, and disease trigger glucocorticoid (GC) elevation. Elevated GCs bind to the ubiquitously expressed glucocorticoid receptor (GR). While GRs are in every cell in the nervous system, the expression level varies, suggesting that diverse cell types react differently to GR activation. Stress/GCs induce structural plasticity in neurons, Schwann cells, microglia, oligodendrocytes, and astrocytes as well as affect neurotransmission by changing the release and reuptake of glutamate. While general nervous system plasticity is essential for adaptation and learning and memory, stress-induced plasticity is often maladaptive and contributes to neuropsychiatric disorders and neuropathic pain. In this brief review, we describe the evidence that stress/GCs activate GR to promote cell type-specific changes in cellular plasticity throughout the nervous system.
压力、损伤和疾病会引发糖皮质激素(GC)的升高。升高的 GC 会与广泛表达的糖皮质激素受体(GR)结合。虽然 GR 存在于神经系统的每个细胞中,但表达水平存在差异,这表明不同的细胞类型对 GR 激活的反应不同。压力/GC 会诱导神经元、许旺细胞、小胶质细胞、少突胶质细胞和星形胶质细胞的结构可塑性,并通过改变谷氨酸的释放和再摄取来影响神经递质传递。虽然一般的神经系统可塑性对于适应、学习和记忆是必不可少的,但应激诱导的可塑性往往是适应不良的,并导致神经精神障碍和神经病理性疼痛。在这篇简要综述中,我们描述了证据表明,压力/GC 通过激活 GR 来促进整个神经系统中细胞类型特异性的细胞可塑性变化。