Increased cerebrospinal fluid glutamate and taurine concentrations are associated with traumatic brain edema formation in rats

Glutamate-mediated excitotoxicity results in cell swelling and contributes to brain edema formation. Since increased extracellular taurine reflects glutamate-induced cell swelling in vitro, elevated CSF taurine could therefore unmask glutamate-mediated cytotoxic edema formation under in vivo conditi...

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Bibliographic Details
Published in:Brain research Vol. 875; no. 1; pp. 51 - 55
Main Authors: Stover, John F., Unterberg, Andreas W.
Format: Journal Article
Language:English
Published: London Elsevier B.V 01-09-2000
Amsterdam Elsevier
New York, NY
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Summary:Glutamate-mediated excitotoxicity results in cell swelling and contributes to brain edema formation. Since increased extracellular taurine reflects glutamate-induced cell swelling in vitro, elevated CSF taurine could therefore unmask glutamate-mediated cytotoxic edema formation under in vivo conditions. For this, the temporal profile of brain edema and changes in cisternal CSF glutamate and taurine levels were determined in 28 rats following focal traumatic brain injury. Compared to six non-traumatized rats, CSF glutamate (4.8±0.3 vs. 10±0.9 μM) and taurine levels (12±1.3 vs. 41±3 μM) were significantly increased at 8 h after trauma ( P<0.001). Over time, CSF glutamate and taurine were significantly increased by 24 (glutamate: 38±4.4 μM) and 48 h (taurine: 51±4 μM), respectively. While CSF glutamate closely reflected changes in hemispheric water content, alterations in CSF taurine occurred diametrically to those seen for glutamate. Under the present study design, increased CSF taurine could reflect glutamate-induced cell swelling. In addition, neuronal release of taurine with its inhibitory and antiexcitotoxic functions could explain the observed diametric changes in CSF glutamate, CSF taurine, and hemispheric water content. Therefore, increasing taurine could be a therapeutic approach in attenuating post-traumatic glutamate-mediated cell damage.
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ISSN:0006-8993
1872-6240
DOI:10.1016/S0006-8993(00)02597-X