Rönnbäck Lars, Johansson Birgitta
Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.
Front Behav Neurosci. 2022 Jan 31;15:791984. doi: 10.3389/fnbeh.2021.791984. eCollection 2021.
Long-lasting mental or cognitive fatigue may be a disabling symptom after physically recovered skull trauma, stroke, infection, or inflammation in the central nervous system (CNS). It is difficult to go back to work and participate in familiar social activities, as typically the person is only able to remain mentally active for short periods, and if mentally exhausted, the recovery time will be disproportionally long. Mental fatigue after traumatic brain injury correlates with brain information processing speed. Information processing is energy consuming and requires widespread and specific neural signaling. Glutamate signaling is essential for information processing, including learning and memory. Low levels and the fine-tuning of extracellular glutamate are necessary to maintain a high precision in information processing. The astroglial cells are responsible for the fine-tuning of the glutamate transmission, but this capacity is attenuated by substances or conditions associated with neuro-inflammation in brain pathology. In this paper, we extend our previously presented hypothesis on the cellular mechanisms underlying mental fatigue suggesting a dysfunction in the astroglial support of the glutamate transmission. Changes in other neurotransmitters such as dopamine, serotonin, norepinephrine, GABA, and acetylcholine after brain injury are also taken into consideration.
在身体从颅骨创伤、中风、感染或中枢神经系统（CNS）炎症中恢复后，长期的精神或认知疲劳可能是一种致残症状。恢复工作和参与熟悉的社交活动变得困难，因为通常情况下，患者只能在短时间内保持精神活跃，而且如果精神疲惫，恢复时间会极长。创伤性脑损伤后的精神疲劳与大脑信息处理速度相关。信息处理需要消耗能量，并且需要广泛而特定的神经信号传导。谷氨酸信号传导对于包括学习和记忆在内的信息处理至关重要。细胞外谷氨酸的低水平及其微调对于维持信息处理的高精度是必要的。星形胶质细胞负责谷氨酸传递的微调，但在脑部病理中，这种能力会因与神经炎症相关的物质或状况而减弱。在本文中，我们扩展了我们之前提出的关于精神疲劳潜在细胞机制的假设，表明谷氨酸传递的星形胶质细胞支持功能存在功能障碍。脑损伤后其他神经递质如多巴胺、血清素、去甲肾上腺素、γ-氨基丁酸和乙酰胆碱的变化也被考虑在内。
