Swanson R A, Choi D W
Department of Neurology, University of California, San Francisco.
J Cereb Blood Flow Metab. 1993 Jan;13(1):162-9. doi: 10.1038/jcbfm.1993.19.
Glia perform several energy-dependent functions that may aid neuronal survival under pathological conditions. Glycogen is the major energy reserve in brain, and it is localized almost exclusively to astrocytes. Using murine cortical cell cultures containing both glia and neurons, we examined the effect of altered glial glycogen stores on neuronal survival following glucose deprivation. As previously reported, cultures exposed for several hours to media lacking glucose developed widespread neuronal degeneration without glial degeneration. If glial astrocyte glycogen content was increased to 2-3 times control levels by a 24-h pretreatment with 1 microM insulin or 0.5 mM methionine sulfoximine (MSO), glucose deprivation-induced neuronal degeneration was attenuated. These protective effects were blocked if glycogen levels were reduced back to control levels by a 30-min exposure to 1 mM dibutyryl cyclic AMP or 20 microM norepinephrine prior to glucose deprivation. Astrocyte glycogen stores may be an important factor influencing neuronal survival under conditions of energy substrate limitation.
神经胶质细胞执行多种依赖能量的功能，这些功能可能有助于在病理条件下神经元的存活。糖原是大脑中的主要能量储备，并且几乎完全定位于星形胶质细胞。我们使用包含神经胶质细胞和神经元的小鼠皮质细胞培养物，研究了在葡萄糖剥夺后，神经胶质细胞糖原储备改变对神经元存活的影响。如先前报道，暴露于缺乏葡萄糖的培养基中数小时的培养物会出现广泛的神经元变性，而神经胶质细胞无变性。如果通过用1微摩尔胰岛素或0.5毫摩尔蛋氨酸亚砜胺（MSO）进行24小时预处理，将神经胶质星形胶质细胞的糖原含量增加至对照水平的2至3倍，则葡萄糖剥夺诱导的神经元变性会减弱。如果在葡萄糖剥夺之前通过暴露于1毫摩尔二丁酰环磷腺苷或20微摩尔去甲肾上腺素30分钟将糖原水平降低至对照水平，则这些保护作用会被阻断。在能量底物受限的条件下，星形胶质细胞的糖原储备可能是影响神经元存活的重要因素。
