The present address of Dr. H. Toki is Department of Otolaryngology, Faculty of Medicine, Hirosaki University, Hirosaki 036, Japan.
Enhancement of Extracellular Glutamate Scavenge System in Injured Motoneurons
Article first published online: 13 NOV 2002
Journal of Neurochemistry
Volume 71, Issue 3, pages 913–919, September 1998
How to Cite
Toki, H., Namikawa, K., Su, Q., Kiryu-Seo, S., Sato, K. and Kiyama, H. (1998), Enhancement of Extracellular Glutamate Scavenge System in Injured Motoneurons. Journal of Neurochemistry, 71: 913–919. doi: 10.1046/j.1471-4159.1998.71030913.x
- Issue published online: 13 NOV 2002
- Article first published online: 13 NOV 2002
- Received December 1, 1997; revised manuscript received March 24, 1998; accepted March 30, 1998.
- Cell death;
- Glutamate transporter;
- Nerve regeneration;
- Glutamate toxicity;
- Glutamate metabolism;
Abstract: An increase in glutamine synthetase (GS) mRNA expression after peripheral motor nerve injury was demonstrated by differential display PCR using single arbitrary primer coupled with in situ hybridization screening called in situ display. Differential display PCR was carried out to compare differences in mRNA expression between axotomized (6 h after the transection) and normal hypoglossal nuclei in mice. Several gene fragments were increased after nerve injury; one was identified as GS. Subsequent emulsion autoradiography of hybridization tissue sections revealed that the increase in GS mRNA was observed in injured motoneurons. As GS is a key enzyme participating in the metabolism of the major excitatory neurotransmitter glutamate, we examined the significance of increased GS expression on glutamate-uptake kinetics. GS-transfected human embryonic kidney cells showed an up-regulation in glutamate-uptake kinetics. Therefore, newly expressed GS together with an increased expression of the neuronal glutamate transporter EAAC1 in the injured motoneurons accelerates glutamate uptake. The present results may suggest that the glutamate-uptake system involving the neuronal glutamate transporter and GS in injured neurons is enhanced so as to provide resistance against neurotoxic glutamate accumulation during the early process of nerve regeneration.