Glucose is the major source of metabolic energy in the peripheral nerv
e. Energy derived from glucose is mostly utilized for axonal repolariz
ation. One route by which glucose may reach the axon is by crossing th
e Schwann cells that initially surround the axons. Considering the abi
lity of neurons to control many glial cell functions, we postulated th
at Schwann cell glucose transporters might be transiently regulated by
axonal contact. Glucose transport was studied in a cultured, differen
tiated rat Schwann cell line stably expressing SV40 T antigen regulate
d by a synthetic mouse metallothionein promoter. (3)[H]-2-deoxy-D-gluc
ose uptake was measured in cultured cells in basal and in various expe
rimental conditions. Glucose transporter gene expression was determine
d after RNA isolation from cultured cells through Northern and RNAse p
rotection assay. In vitro, Schwann cells were found to express high-af
finity, insulin-insensitive, facilitative glucose transporters and pre
dominantly GLUT1 mRNA. Schwann cell 2-deoxyglucose uptake was increase
d by axolemmal membranes or forskolin but unchanged by elevated glucos
e levels. Regulation of Schwann cell glucose transporters by axolemma
and their resistance to glucose-induced down-regulation suggest extrin
sic rather than intrinsic regulation that might enhance Schwann cell v
ulnerability to glucotoxicity.