TNF-NF-κB signaling mediates excessive somnolence in hemiparkinsonian rats

A review of the neuro- and systemic inflammatory responses in post concussion symptoms: Introduction of the “post-inflammatory brain syndrome” PIBS

“…In atopic dermatitis, the chemokine CCL18 is associated with the symptom of sleep loss (Hon et al, 2011). In Parkinson's disease TNF-a levels correlate with sleep disturbances (Menza et al, 2010), which is expected given that TNF-a expression increased in rats with induced hemiparkinsonianism and TNF-a receptor fragment administration prevented sleep changes in these rats (Lu et al, 2010). Similar results being seen with induced parkinsonism with Il-1b levels in the hypothalamus and IL-1ra (Yi et al, 2007).…”

Original article Nigrostriatal pathway degeneration in rats after intraperitoneal administration of proteasome inhibitor MG-132

“…Some authors [31,33] indicate that systematically administered proteasome inhibitors may penetrate the intact blood-brain barrier and cause pathological changes in the central nervous system (CNS), leading also to locomotor dysfunction and behavioural disturbances. It has also been reported that MG-132-induced hemiparkinsonism in the rat model mimics the daytime somnolence and sleep disturbance during the night observed in patients with the Parkinson's disease [26]. To date, there have been no reports describing the long-term effects of MG-132 on the CNS structures after its administration by intraperitoneal route.…”

Biphasic effects of baicalin, an active constituent of Scutellaria baicalensis Georgi, in the spontaneous sleep–wake regulation

“…Our previous studies have also demonstrated that the increase of proinflammatory cytokines, e.g. IL-1 and TNF-␣, after microglial activation in Parkinsonism rats is dominant in the sleep disruption (Yi et al, 2007;Lu et al, 2010). Thus, the anti-inflammatory feature of baicalin may alter spontaneous sleep-wake activity.…”

“…IL-1␤ administered centrally into rats during their active period (dark period) is particularly effective in increasing SWS and reducing waking (Opp and Krueger, 1992;Krueger and Fang, 1999). Besides their effects on physiological sleep regulation, proinflammatory cytokines, including IL-1␤ and TNF-␣, have previously depicted the implication of pathological sleep disruption caused by neurological diseases, such as epilepsy and Parkinson's disease (Yi et al, 2004(Yi et al, , 2007Lu et al, 2010). Because the expression of IL-1␤ is highest during the light period and baicalin possesses the ability to suppress IL-1's effect (as aforementioned), we speculated that the baicalin-induced SWS decrement during the first 2 h of the light period is due to the blockade of IL-1 receptors, the decrease of IL-1 production, or both.…”