Abstract
Glutamate is a major excitatory transmitter in the central nervous system that may produce cellular injury when its concentration is abnormally increased in the synaptic cleft. Glial glutamate transporters GLAST and GLT-1, which are responsible for clearing synaptic glutamate into glial cells, play an important role in the regulation of the glutamate concentration in the synaptic cleft. However, there has been no report on long-term changes in the levels of glutamate transporters following spinal cord injury. Spinal cord injury (SCI) was induced at T12 by a New York University (NYU) impactor. Segments of the spinal cord at T9-10, L1-2, L4-5 and at the epicenter were removed after SCI, and Western blots for GLAST, GLT-1 and EAAC1 were performed. GLAST and GLT-1 were significantly decreased in the epicenter from 1 day up to 8 weeks after SCI. GLT-1 was significantly decreased in the spinal segments rostral to the injury site, and GLAST expression was significantly increased in the L4-5 region of the spinal cord for 8 weeks. Because strategies to modulate the regulation of glutamate transporters may be applied, the present data serve as a reference for further research, although the long-term roles of glutamate transporters in pathological processes caused by SCI are not clear.
Original language | English |
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Pages (from-to) | 194-199 |
Number of pages | 6 |
Journal | Brain Research |
Volume | 1389 |
DOIs | |
Publication status | Published - 2011 May 10 |
Keywords
- Glutamate
- Glutamate transporter
- Spinal cord injury
ASJC Scopus subject areas
- Neuroscience(all)
- Molecular Biology
- Clinical Neurology
- Developmental Biology