Departamento de Medicina y Cirugía Animal, Universidad CEU Cardenal Herrera, Moncada (Valencia), Spain.
J Anat. 2011 Oct;219(4):525-30. doi: 10.1111/j.1469-7580.2011.01410.x. Epub 2011 Jul 11.
Peripheral nerve axotomy in adult mice elicits a complex response that includes increased glucose uptake in regenerating nerve cells. This work analyses the expression of the neuronal glucose transporters GLUT3, GLUT4 and GLUT8 in the facial nucleus of adult mice during the first days after facial nerve axotomy. Our results show that whereas GLUT3 levels do not vary, GLUT4 and GLUT8 immunoreactivity increases in the cell body of the injured motoneurons after the lesion. A sharp increase in GLUT4 immunoreactivity was detected 3 days after the nerve injury and levels remained high on Day 8, but to a lesser extent. GLUT8 also increased the levels but later than GLUT4, as they only rose on Day 8 post-lesion. These results indicate that glucose transport is activated in regenerating motoneurons and that GLUT4 plays a main role in this function. These results also suggest that metabolic defects involving impairment of glucose transporters may be principal components of the neurotoxic mechanisms leading to motoneuron death.
成年小鼠周围神经轴突切断后会引发一系列复杂反应,包括再生神经细胞的葡萄糖摄取增加。本研究分析了面神经轴突切断后最初几天成年小鼠面神经核中神经元葡萄糖转运体 GLUT3、GLUT4 和 GLUT8 的表达。结果表明,损伤后神经元胞体中 GLUT3 水平没有变化,而 GLUT4 和 GLUT8 的免疫反应性增加。神经损伤后 3 天检测到 GLUT4 免疫反应性急剧增加,第 8 天仍保持高水平,但程度较低。GLUT8 也增加了水平,但比 GLUT4 晚,因为它们仅在损伤后第 8 天上升。这些结果表明,葡萄糖转运在再生运动神经元中被激活,GLUT4 在该功能中起主要作用。这些结果还表明,涉及葡萄糖转运体功能障碍的代谢缺陷可能是导致运动神经元死亡的神经毒性机制的主要组成部分。