Blood–Brain Barrier Dysfunction Predicts Microglial Activation After Traumatic Brain Injury in Juvenile Rats

• DOI: 10.1089/neur.2023.0057
• Publication Date: 2024-02-08T22:18:28Z
• Authors: Tabitha R.F. Green; Tina Nguyen; Veronika Dunker; Danielle Ashton; J. Bryce Ortiz; Sean M. Murphy; Rachel K. Rowe
• Keywords: pediatric; vasculature; RC86-88.9; concussion; Medical emergencies. Critical care. Intensive care. First aid; Original Article; neuroinflammation

Traumatic brain injury (TBI) disrupts the blood–brain barrier (BBB), which may exacerbate neuroinflammation post-injury. Few translational studies have examined BBB dysfunction and subsequent post-TBI in juveniles. We hypothesized that positively predicts microglial activation vulnerability to associated are dependent on age at injury. Post-natal day (PND)17 PND35 rats (n = 56) received midline fluid percussion or sham surgery, immunoglobulin-G (IgG) stain was quantified as a marker of extravasated blood dysfunction. investigated response hippocampus, hypothalamus, motor cortex relative days post-injury (DPI; 1, 7, 25). measured morphologies ionized calcium-binding adaptor molecule 1–labeled microglia using cell body area perimeter, branch number length, end-points/microglial cell, microglia. Data were analyzed generalized hierarchical models. In PND17 rats, TBI increased levels IgG compared shams. Independent injury, higher 1 7 DPI, but resolved by 25 DPI. activated (more cells fewer end-points) respective induced morphological changes indicative activation, had end-points per DPI than TBI, larger, more rats; larger areas perimeters rats. Importantly, we found support both ages quantification predicted after TBI. The with increasing IgG, whereas length decreased together indicate activation. Our results suggest stabilization pediatric be an important therapeutic strategy limit promote recovery.