Expression of SOD1 G93A or wild-type SOD1 in primary cultures of astrocytes down-regulates the glutamate transporter GLT-1: lack of involvement of oxidative stress.

@article{Tortarolo2004ExpressionOS,
  title={Expression of SOD1 G93A or wild-type SOD1 in primary cultures of astrocytes down-regulates the glutamate transporter GLT-1: lack of involvement of oxidative stress.},
  author={Massimo Tortarolo and Andrew J Crossthwaite and Laura Conforti and Jeremy P. E. Spencer and Robert J Williams and Caterina Bendotti and Marcus Rattray},
  journal={Journal of neurochemistry},
  year={2004},
  volume={88 2},
  pages={481-93}
}
Glutamate excitotoxicity is implicated in the aetiology of amyotrophic lateral sclerosis (ALS) with impairment of glutamate transport into astrocytes a possible cause of glutamate-induced injury to motor neurons. It is possible that mutations of Cu/Zn superoxide dismutase (SOD1), responsible for about 20% of familial ALS, down-regulates glutamate transporters via oxidative stress. We transfected primary mouse astrocytes to investigate the effect of the FALS-linked mutant hSOD1(G93A) and wild… CONTINUE READING