title: Changes of retinal glutamate transporter GLT-1 mRNA levels following optic nerve damage.
abstract: OBJECTIVE
  Under physiological conditions, levels of the excitatory neurotransmitter glutamate within the retina are regulated by retinal glutamate transporters to prevent toxic accumulation. Alterations in this glutamate buffering have been implicated in retinal ganglion cell (RGC) death. We quantified the changes in the level of glutamate transporter mRNA in a model of acute rat optic nerve injury.
  
  
  METHODS
  Optic nerve damage was induced in one eye of 25 adult Wistar rats by partial optic nerve crush (ONC). Total mRNA levels of the retinal glutamate transporter GLT-1 (EAAT-2) were determined by quantitative real-time PCR. GLT-1 mRNA levels were measured 1, 3, 7, 14, and 28 days following optic nerve injury. Additionally, control values were obtained from the retinas of five control rats (sham-crush).
  
  
  RESULTS
  In the very early phase (1 day post-ONC), a 3.9 fold increase in levels of GLT-1 mRNA was observed in the ONC retinae compared with control eyes. This was followed by a rapid decrease towards control levels at day 3 post-ONC. GLT-1 mRNA levels remained up to 14 days post-crush. However, in the late phase post-ONC (day 28), the level of GLT-1 mRNA increased again, but still remained not significant to control levels.
  
  
  CONCLUSIONS
  Changes in GLT-1 mRNA expression following axonal trauma of RGCs can lead to an imbalance of glutamate homeostasis. This may cause local accumulation of toxic concentrations of the neurotransmitter glutamate and further irreversible excitotoxic damage of RGCs.
authors.affiliation: Department of Neuropathology, Otto-von-Guericke-University, Magdeburg, Germany.
authors.forename: Christian
authors.initials: C
authors.lastname: Mawrin
authors.forename: Thomas
authors.initials: T
authors.lastname: Pap
authors.forename: Martina
authors.initials: M
authors.lastname: Pallas
authors.forename: Knut
authors.initials: K
authors.lastname: Dietzmann
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Behrens-Baumann
authors.forename: Christian K
authors.initials: CK
authors.lastname: Vorwerk
mesh_terms: D000818:Animals; D016923:Cell Death; D017931:DNA Primers / Q000737:chemistry; D015536:Down-Regulation; D027342:Excitatory Amino Acid Transporter 2 / Q000235:genetics* / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D006706:Homeostasis; D023421:Models, Animal; D009409:Nerve Crush; D020221:Optic Nerve Injuries / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D012160:Retina / Q000378:metabolism* / Q000473:pathology; D012165:Retinal Ganglion Cells / Q000473:pathology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015854:Up-Regulation
chemical_list: D017931:DNA Primers; D027342:Excitatory Amino Acid Transporter 2; D012333:RNA, Messenger; D018698:Glutamic Acid