Assessment of mouse cognitive and anxiety-like behaviors and hippocampal inflammation following a repeated and intermittent paradoxical sleep deprivation procedure

The spleen mediates chronic sleep restriction-mediated enhancement of LPS-induced neuroinflammation, cognitive deficits, and anxiety-like behavior

“…First, we studied the effects of CRSR on cognitive deficits and anxiety-like behavior in the LPS-induced systemic inflammation mouse model. The open field test (OFT) and Y maze test (YMT) can successfully detect anxiety-like behavior and working memory dysfunctions in mice [ 24 ]. Two-way ANOVA analysis of Y maze test data showed that CRSR decreased number of entries (CRSR: F 1,20 = 6.206, P = 0.0216; LPS: F 1,20 = 20.54, P = 0.0002; interaction (CRSR × LPS): F 1,20 = 0.4226, P = 0.5230) and time spent in the novel arm (CRSR: F 1,20 = 7.014, P = 0.0154; LPS: F 1,20 = 21.21, P = 0.0002; interaction (CRSR × LPS): F 1,20 = 0.5378, P = 0.4719) compared to the non-CRSR group in LPS-treated mice, but not in saline-treated mice ( Figure 1B , 1C ).…”

“…Accumulating evidence indicates that acute short-term or chronic long-term sleep disruption, which are widespread in modern society, can cause systemic inflammation, cellular and humoral immune system dysfunction, and neuroinflammatory responses [ 12 , 15 , 24 , 32 ], which collectively can promote synapse loss, mood disorders, cognitive impairment, and neurodegenerative and neurobehavioral diseases [ 12 – 15 ]. Short-term sleep restriction for 3 days increases TNF-α, IL-6, and IL-1β levels in hippocampus and basal forebrain [ 32 ].…”

“…Chronic sleep deprivation for 21 consecutive days also markedly increased TNF-α and IL-6 expression in hippocampus [ 15 ]. However, IL-1β and IL-6 protein expression were not elevated in the hippocampus three weeks after three months of repeated intermittent paradoxical sleep deprivation [ 24 ]. Similarly, we found in the present study that plasma and hippocampal levels of TNF-α, IL-6, IL-17A, and IFN-γ were not increased 2 weeks after CRSR compared to non-CRSR control mice, indicating that the enhancing effects of CRSR on LPS-induced neuroinflammatory damage were not associated with pre-existing inflammatory response status.…”

Indole-3-guanylhydrazone hydrochloride mitigates long-term cognitive impairment in a neonatal sepsis model with involvement of MAPK and NFκB pathways

“…Several studies have attributed the long-term cognitive impairment and anxiety-like the behavior of septic mice to the to the brain inflammation (Chesnokova et al, 2016;Yin et al, 2017) that occurred during neonatal phase. A common feature of neonatal sepsis is the systemic induction of inflammatory mediators, which can disrupt the blood-brain barrier (BBB) and interact with the brain, thereby causing brain inflammation.…”

Prefrontal dopamine D1 receptor manipulation influences anxiety behavior and induces neuroinflammation within the hippocampus

“…An additional potential mechanism of action is enhanced hippocampal neurogenesis (Liu et al 2016). Also other manipulations can affect in ammation and induce anxiety and depression-like behavior in rodents, such as sleep deprivation (Wadhwa et al 2018;Yin et al 2017;Zielinski et al 2014), chronic mild stress (Wang et al 2018;You et al 2011) and models for chronic in ammatory disease, like diabetes or metabolic syndrome (de Cossío et al Dinel et al 2011;Zhou et al 2018). All those ndings share, that increased in ammation in the hippocampus induces anxiety and depression-like behavior in rodents, and those behavioral symptoms could be attenuated through anti-in ammatory agents which reduced among other pro-in ammatory cytokines IL-6.…”