Data from: Age-at-injury influences the glial response to traumatic brain injury in the cortex of male juvenile rats

Glia influence neuronal development and aging. Few translational studies
have examined how age at injury affects the glial response to traumatic
brain injury (TBI). We hypothesized that rats injured before sexual
maturity would exhibit a greater glial response, that persists into early
adulthood, compared to rats injured near the onset of sexual maturity.
Postnatal day (PND)17 and PND35 rats received midline fluid percussion
injury or sham surgery. In three cortical regions (peri-injury, S1BF,
perirhinal), we investigated the glial response relative to age at injury,
time post-injury (2H, 1D 7D, 25D, and 43D), and post-natal age, such that
rats injured at PND17 or PND35 were compared at the same post-natal-age
(e.g., PND17+25d post-injury=PND42; PND35+7d post-injury=PND42). We
measured Iba1+ microglia cells and quantified their activation status.
GFAP expression was examined using immunohistochemistry. Data were
analyzed using Bayesian multivariate multi-level models. Independent of
age at injury, TBI activated microglia (shorter branches, fewer endpoints)
in the cortex with more microglia in all regions compared to shams.
TBI-induced microglial activation was sustained in the S1BF into early
adulthood (PND60). PND17 injured rats had more microglial activation in
the perirhinal cortex than PND35 injured rats. Activation was not
confounded by age-dependent cell size changes, and microglial cell body
sizes were similar between ages. Increased microglial activation in PND17
injured rats suggests that TBI upregulates the glial response at discrete
stages of development. Age at injury and aging with an injury are
translationally important because experiencing a TBI during early
childhood may trigger an exaggerated glial response.