β2 Adrenergic-mediated Reduction of Blood Glutamate Levels and Improved Neurological Outcome After Traumatic Brain Injury in Rats

Abstract

The results suggest that the transient blood glutamate reduction seen after TBI is the result of a stress response and of the activation of the sympathetic nervous system through the β2 adrenergic receptors, causing an increase of the brain-to-blood efflux of glutamate observed with excess brain glutamate levels after a brain insult. This strongly correlates with the neurological improvement observed 24 hours after TBI.