Traumatic brain injury induces region-specific glutamate metabolism changes as measured by multiple mass spectrometry methods.

ABSTRACT: The release of excess glutamate following traumatic brain injury (TBI) results in glutamate excitotoxicity and metabolic energy failure. Endogenous mechanisms for reducing glutamate concentration in the brain parenchyma following TBI are poorly understood. Using multiple mass spectrometry approaches, we examined TBI-induced changes to glutamate metabolism. We present evidence that glutamate concentration can be reduced by glutamate oxidation via a "truncated" tricarboxylic acid cycle coupled to the urea cycle. This process reduces glutamate levels, generates carbon for energy metabolism, leads to citrulline accumulation, and produces nitric oxide. Several key metabolites are identified by metabolomics in support of this mechanism and the locations of these metabolites in the injured hemisp

SUBMITTER: Sowers JL 

PROVIDER: S-EPMC8479783 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature