Blast Exposure Induces Acute Alterations in Circadian Clock Genes in the Hypothalamus and Pineal Gland in Rats: An Exploratory Study

Govindarajulu, Manoj; Patel, Mital Y.; Krishnan, Jishnu; Long, Joseph B.; Arun, Peethambaran

doi:10.1089/neur.2023.0048

Cited by 1 publication

(1 citation statement)

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“…These findings are consistent with studies of increased sleepiness after TBI in humans and level of TBI severity with IL-1β potentially increasing sleepiness after injury ( Watson et al, 2007 ). Cellular and molecular mechanisms other than those involving inflammation can also contribute to the sleep effects, such as loss of hypocretin neurons post-TBI ( Thomasy and Opp, 2019 ), changes in hypocretin ligands and receptors ( Korthas et al, 2022 ), and changes in circadian gene expression (e.g., Clock, Per1, Per 2, Bmal, Cry1, Cry2 ; Boone et al, 2012 ; Govindarajulu et al, 2023 ).…”

Section: Tbi-induced Mechanisms That Dysregulate Sleepmentioning

confidence: 99%

Sleep, inflammation, and hemodynamics in rodent models of traumatic brain injury

Green,

Carey,

Mannino

et al. 2024

Front. Neurosci.

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Traumatic brain injury (TBI) can induce dysregulation of sleep. Sleep disturbances include hypersomnia and hyposomnia, sleep fragmentation, difficulty falling asleep, and altered electroencephalograms. TBI results in inflammation and altered hemodynamics, such as changes in blood brain barrier permeability and cerebral blood flow. Both inflammation and altered hemodynamics, which are known sleep regulators, contribute to sleep impairments post-TBI. TBIs are heterogenous in cause and biomechanics, which leads to different molecular and symptomatic outcomes. Animal models of TBI have been developed to model the heterogeneity of TBIs observed in the clinic. This review discusses the intricate relationship between sleep, inflammation, and hemodynamics in pre-clinical rodent models of TBI.

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