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

J Anat. 2011 Oct;219(4):525-30. doi: 10.1111/j.1469-7580.2011.01410.x. Epub 2011 Jul 11.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Axotomy
  • Facial Nerve / metabolism*
  • Facial Nerve / surgery
  • Facial Nerve Injuries / metabolism*
  • Glucose Transport Proteins, Facilitative / metabolism*
  • Glucose Transporter Type 4 / metabolism*
  • Mice
  • Mice, Inbred C57BL
  • Nerve Regeneration*
  • Up-Regulation

Substances

  • Glucose Transport Proteins, Facilitative
  • Glucose Transporter Type 4
  • Slc2a4 protein, mouse
  • Slc2a8 protein, mouse