Region-Dependent Modulation of Neural Plasticity in Limbic Structures Early after Traumatic Brain Injury

Traumatic brain injury (TBI)-induced disruptions in synaptic function within regions and across networks the limbic system may underlie a vulnerability for maladaptive plasticity contribute to behavioral comorbidities. In this study we measured how proteins respond lateral fluid percussion (FPI) known regulate emotion memory, including basolateral amygdala (BLA), dorsal ventral hippocampus (DH, VH), medial prefrontal cortex (PFC). We investigated involved regulating plasticity, glutamatergic a-amino-3-hydroxy5-methyl-4-isoxazolepropionic acid (AMPA; GluA1, GluA2) N-methyl-D-aspartate (NMDA; NR1, NR2A, NR2B) receptor subunits as well inhibitory gamma-aminobutyric (GABA) synthetic enzymes (GAD67, GAD65) via western blot. Adult male rats received mild-moderate FPI or sham surgery ipsi- contralateral BLA, DH, VH, PFC were collected 6 h, 24 48 7 days post-injury. ipsilateral there was significant decrease NR1 GluA2 h after injury, whereas NR2A NR2B increased BLA at compared with sham. GAD67 ipsilaterally but decreased contralaterally BLA. both NMDA (NR2A, GABA-synthetic (GAD65, GAD67) acutely also robustly VH h. significantly between FPI, GAD65 same time-points VH. saw bilateral increases GluA1. Later, from Collectively, these data suggest that causes dynamic homeostatic response networks, leading an imbalance of neural systems underlying cognitive emotional regulation.