Investigating neuroinflammation in lateral fluid percussion injury

Tapp, Zoe; Kokiko-Cochran, Olga N.

doi:10.1016/b978-0-323-89833-1.00023-9

Cited by 1 publication

(1 citation statement)

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“… 1 Chronic, maladaptive neuroinflammation has been a focus of both pre-clinical and clinical neurotrauma research as a major propagator of long-term impairment. 2 , 3 Previous work shows that chronic reactivity of the resident brain macrophage, microglia, is associated with lasting cognitive deficits in TBI survivors. 4 This is recapitulated in experimental models of TBI given that depletion or turnover of microglia after injury attenuates neuroinflammation, improves neuronal function, and rescues behavioral deficits.…”

Section: Introductionmentioning

confidence: 99%

Divergent Spatial Learning, Enhanced Neuronal Transcription, and Blood–Brain Barrier Disruption Develop During Recovery from Post-Injury Sleep Fragmentation

Tapp,

Ren,

Palmer

et al. 2023

Neurotrauma Reports

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Traumatic brain injury (TBI) causes pathophysiology that may significantly decrease quality of life over time. A major propagator of this response is chronic, maladaptive neuroinflammation, which can be exacerbated by stressors such as sleep fragmentation (SF). This study determined whether post-TBI SF had lasting behavioral and inflammatory effects even with a period of recovery. To test this, male and female mice received a moderate lateral fluid percussion TBI or sham surgery. Half the mice were left undisturbed, and half were exposed to daily SF for 30 days. All mice were then undisturbed between 30 and 60 days post-injury (DPI), allowing mice to recover from SF (SF-R). SF-R did not impair global Barnes maze performance. Nonetheless, TBI SF-R mice displayed retrogression in latency to reach the goal box within testing days. These nuanced behavioral changes in TBI SF-R mice were associated with enhanced expression of neuronal processing/signaling genes and indicators of blood–brain barrier (BBB) dysfunction. Aquaporin-4 (AQP4) expression, a marker of BBB integrity, was differentially altered by TBI and TBI SF-R. For example, TBI enhanced cortical AQP4 whereas TBI SF-R mice had the lowest cortical expression of perivascular AQP4, dysregulated AQP4 polarization, and the highest number of CD45 + cells in the ipsilateral cortex. Altogether, post-TBI SF caused lasting, divergent behavioral responses associated with enhanced expression of neuronal transcription and BBB disruption even after a period of recovery from SF. Understanding lasting impacts from post-TBI stressors can better inform both acute and chronic post-injury care to improve long-term outcome post-TBI.

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