Traumatic brain injury, alone or with striatal hemorrhage-like extension, transiently decreases GABA and glutamate levels along motor deficits in the rat striatum: an in vivo study.

The cerebral cortex is connected to the striatum via the axons of the pyramidal glutamatergic neurons, and this pathway is intimately involved in motor function. In the striatum, glutamatergic afferents initiate the activity of GABAergic medium spiny neurons. This study addressed whether traumatic brain injury (TBI) affects GABA and glutamate extracellular levels in the dorsal striatum as an indicator of effects on the cortico-striatal pathway, in rats with motor deficits and recovered animals. Animals were assigned to a sham group, a TBI-alone group, and a TBI + striatal injury group (local injection of a FeCl2 solution to mimic hemorrhagic lesion). In the TBI-alone and TBI + striatal injury groups, motor deficits were accompanied by decreased extracellular GABA and glutamate levels in the striatum at 3 days post-injury. The TBI + striatal injury group showed higher motor deficits, which lasted 7 days longer, and GABA levels were significantly different compared to the TBI alone group. At 18 days post-injury, in recovered rats from the TBI-alone group GABA and glutamate levels returned to control levels. Alterations in extracellular GABA and glutamate levels indicate damage to the cortico-striatal pathway, underscoring the importance of studying this pathway for treatment and recovery after TBI.