TY  - JOUR
Y1  - 2010///
SP  - 1101
A1  -  Nagy Dávid
A1  -  Knapp Levente
A1  -  Marosi Máté Gábor
A1  -  Farkas Tamás
A1  -  Kis Zsolt
A1  -  Vécsei László
A1  -  Teichberg Vivian I.
A1  -  Toldi József
N1  - FELTÖLT?: Gyengéné Ruszka Marian - gyengeneruszka@freemail.hu
UR  - http://publicatio.bibl.u-szeged.hu/9929/
ID  - publicatio9929
EP  - 1106
SN  - 0272-4340
PB  - Springer
IS  - 7
TI  - Effects of Blood Glutamate Scavenging on Cortical Evoked Potentials
JF  - CELLULAR AND MOLECULAR NEUROBIOLOGY
VL  - 30
N2  - It is well known that traumatic or ischemic brain injury is followed by acute excitotoxicity caused by the presence of abnormally high glutamate (Glu) in brain fluids. It has recently been demonstrated that excess Glu can be eliminated from brain into blood following the intravenous administration of oxaloacetate (OxAc), which, by scavenging blood Glu, induces an enhanced and neuroprotective brain-to-blood Glu efflux. In this study, we subjected rats to intravenous OxAc administration (i.v., 12.5, 25, and 50 mg/kg, respectively), and studied its effects on somatosensory evoked cortical potentials (EPs). Against our expectation, the amplitudes of EPs did not decrease but increased in a dose- and time-dependent manner after OxAc administration. Similar effects were observed when blood Glu scavenging was enhanced by combining OxAc (12.5 mg/kgbw) with recombinant glutamate-oxaloacetate transaminase (GOT, 0.14 nmol/100 g rat). On the basis of these results, we suggest that the changes of amplitudes of the EPs involve not only a glutamatergic but also the weakening of a GABAergic component. We cannot rule out the possibility that OxAc penetrates into the brain and improves mitochondrial functions.
AV  - restricted
ER  -