By Yara Alfawares, Biological Sciences and Neurobiology
Advisor: Laura Ngwenya
Abstract: Spreading depolarizations (SD) occur in 50-60% of patients with traumatic brain injury (TBI) and contribute to secondary brain injury. SDs cause acute changes in glutamate but their effects on glutamatergic receptors is unknown. The study glutamate receptor examines expression after SDs and hypothesizes that cortical and hippocampal SDs will have both local and distant effects. SDs were induced in either the frontal cortex (CSD) or the hippocampus (HSD). CSDs were recorded in the parietal cortex. N-methyl-D-aspartate (NMDA) receptor subunits GluN2a and GluN2b, and _-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunits GluA1 and GluA2 were examined in hippocampal, and frontal and parietal cortical tissue. There was a significant increase in GluA1 (p=0.0233) and GluN2a (p=0.0028) in hippocampal tissue of HSD animals compared to controls; yet, HSD animals had significantly decreased GluA2 (p=0.0253) levels in hippocampal tissue compared to CSD. GluN2b levels in parietal cortical tissue were significantly increased in HSD animals compared to both controls (p=0.0005) and CSDs (p=0.0309), a distant effect. GluA2 levels were significantly lower in HSD frontal cortical tissue compared to both CSD (p=0.0052) and Sham (p=0.0014), another distant effect. We found that SDs do initiate glutamatergic receptor subunit changes. The results imply that SDs can have distant effects on protein expression. Further research is needed to determine whether these changes persist in the injured brain, and can be used as a target for patient-centered treatment.