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首页> 外文期刊>Journal of Neurochemistry: Offical Journal of the International Society for Neurochemistry >Bioenergetics and redox adaptations of astrocytes to neuronal activity
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Bioenergetics and redox adaptations of astrocytes to neuronal activity

机译：星形胶质细胞对神经元活性的生物能和氧化还原适应

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摘要

Neuronal activity is a high-energy demanding process recruiting all neural cells that adapt their metabolism to sustain the energy and redox balance of neurons. During neurotransmission, synaptic cleft glutamate activates its receptors in neurons and in astrocytes, before being taken up by astrocytes through energy costly transporters. In astrocytes, the energy requirement for glutamate influx is likely to be met by glycolysis. To enable this, astrocytes are constitutively glycolytic, robustly expressing 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 (PFKFB3), an enzyme that is negligibly present in neurons by continuous degradation because of the ubiquitin-proteasome pathway via anaphase-promoting complex/cyclosome (APC)-Cdh1. Additional factors contributing to the glycolytic frame of astrocytes may include 5-AMP-activated protein kinase (AMPK), hypoxia-inducible factor-1 (HIF-1), pyruvate kinase muscle isoform-2 (PKM2), pyruvate dehydrogenase kinase-4 (PDK4), lactate dehydrogenase-B, or monocarboxylate transporter-4 (MCT4). Neurotransmission-associated messengers, such as nitric oxide or ammonium, stimulate lactate release from astrocytes. Astrocyte-derived glycolytic lactate thus sustains the energy needs of neurons, which in contrast to astrocytes mainly rely on oxidative phosphorylation. Neuronal activity unavoidably triggers reactive oxygen species, but the antioxidant defense of neurons is weak; hence, they use glucose for oxidation through the pentose-phosphate pathway to preserve the redox status. Furthermore, neural activity is coupled with erythroid-derived erythroid-derived 2-like 2 (Nrf2) mediated transcriptional activation of antioxidant genes in astrocytes, which boost the denovo glutathione biosynthesis in neighbor neurons. Thus, the bioenergetics and redox programs of astrocytes are adapted to sustain neuronal activity and survival. Developing therapeutic strategies to interfere with these pathways may be useful to combat neurological diseases.
机译：神经元活动是一个高能量需求过程，需要募集所有适应其新陈代谢以维持神经元能量和氧化还原平衡的神经细胞。在神经传递过程中，突触裂谷氨酸在神经元和星形胶质细胞中激活其受体，然后被能量成本高昂的转运蛋白所吸收。在星形胶质细胞中，糖酵解可能会满足谷氨酸流入的能量需求。为此，星形胶质细胞具有组成性的糖酵解作用，能强烈表达6-磷酸果糖-2-激酶/果糖-2,6-双磷酸酶-3（PFKFB3），该酶由于遍在蛋白-蛋白酶体途径而通过连续降解而在神经元中微不足道。通过后期促进复合物/环体（APC）-Cdh1。有助于星形胶质细胞糖酵解框架的其他因素可能包括5-AMP激活的蛋白激酶（AMPK），缺氧诱导因子1（HIF-1），丙酮酸激酶肌肉亚型2（PKM2），丙酮酸脱氢酶激酶4（ PDK4），乳酸脱氢酶B或单羧酸盐转运蛋白4（MCT4）。与神经传递相关的信使，例如一氧化氮或铵，刺激星形胶质细胞释放乳酸。因此，星形胶质细胞衍生的糖酵解乳酸盐维持了神经元的能量需求，与星形胶质细胞相反，星形胶质细胞主要依靠氧化磷酸化。神经元的活动不可避免地会触发活性氧，但是神经元的抗氧化防御能力很弱。因此，他们使用葡萄糖通过戊糖-磷酸途径进行氧化，以保持氧化还原状态。此外，神经活动与类红细胞衍生的类红细胞衍生的2-样2（Nrf2）介导的星形胶质细胞中抗氧化剂基因的转录激活相关联，从而增强了相邻神经元中的谷胱甘肽谷胱甘肽的生物合成。因此，星形胶质细胞的生物能和氧化还原程序适合维持神经元的活动和生存。制定治疗策略来干扰这些途径可能有助于对抗神经系统疾病。

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