Effects of Blood Glutamate Scavenging on Cortical Evoked Potentials
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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.
KeywordsNeurotoxicity Neuroprotection Brain glutamate levels Glutamate Oxaloacetate Glutamate–oxaloacetate transaminase Glutamate scavenging Evoked potential Somatosensory cortex
This study was supported by the OTKA K75628. FT is a Bolyai Fellow of the Hungarian Academy of Sciences. V.I.T. has received support from Nella and Leon Benoziyo Center for Neurological Diseases at the Weizmann Institute.
No conflicting financial interests exist.
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