Glucose transporters GLUT4 and GLUT8 are upregulated after facial nerve axotomy in adult mice

被引:11
|
作者
Gomez, Olga [1 ]
Ballester-Lurbe, Begona [2 ]
Mesonero, Jose E. [3 ]
Terrado, Jose [1 ]
机构
[1] Univ CEU Cardenal Herrera, Fac Vet, Dept Med & Cirugia Anim, Moncada 46113, Valencia, Spain
[2] Univ CEU Cardenal Herrera, Dept Quim Bioquim & Biol Mol, Fac Ciencias Expt & Salud, Moncada 46113, Valencia, Spain
[3] Univ Zaragoza, Fac Vet, Unidad Fisiol, Dept Farmacol & Fisiol, Zaragoza, Spain
关键词
glucose transport; GLUT; motoneuron; nerve lesion; neuron; DEVELOPMENTAL REGULATION; DIFFERENTIAL EXPRESSION; HYPOGLOSSAL NUCLEUS; INSULIN; BRAIN; GROWTH; TRANSLOCATION; LOCALIZATION; NEURONS;
D O I
10.1111/j.1469-7580.2011.01410.x
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 ;
摘要
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.
引用
收藏
页码:525 / 530
页数:6
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