Bambrick Linda, Kristian Tibor, Fiskum Gary
Department of Anesthesiology, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, Maryland 21201, USA.
Neurochem Res. 2004 Mar;29(3):601-8. doi: 10.1023/b:nere.0000014830.06376.e6.
Research on ischemic brain injury has established a central role of mitochondria in neuron death. Astrocytes are also damaged by ischemia, although the participation of mitochondria in their injury is ill defined. As astrocytes are responsible for neuronal metabolic and trophic support, astrocyte dysfunction will compromise postischemic neuronal survival. Ischemic alterations to astrocyte energy metabolism and the uptake and metabolism of the excitatory amino acid transmitter glutamate may be particularly important. Despite the significance of ischemic astrocyte injury, little is known of the mechanisms responsible for astrocyte death and dysfunction. This review focuses on differences between astrocyte and neuronal metabolism and mitochondrial function, and on neuronal-glial interactions. The potential for astrocyte mitochondria to serve as targets of neuroprotective interventions is also discussed.
对缺血性脑损伤的研究已证实线粒体在神经元死亡中起核心作用。星形胶质细胞也会因缺血而受损,尽管线粒体在其损伤中的参与情况尚不明确。由于星形胶质细胞负责神经元的代谢和营养支持,星形胶质细胞功能障碍将危及缺血后神经元的存活。星形胶质细胞能量代谢的缺血性改变以及兴奋性氨基酸递质谷氨酸的摄取和代谢可能尤为重要。尽管缺血性星形胶质细胞损伤具有重要意义,但对导致星形胶质细胞死亡和功能障碍的机制却知之甚少。本综述重点关注星形胶质细胞与神经元代谢及线粒体功能之间的差异,以及神经元与神经胶质细胞的相互作用。还讨论了星形胶质细胞线粒体作为神经保护干预靶点的可能性。