Behavioural brain research
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Sleep disturbance can result in memory impairment, and both sleep and hippocampal memory formation are maintained by circadian clock genes. Although preoperative sleep deprivation is known to be an independent risk factor for postoperative cognitive dysfunction (POCD) after inhalation anesthesia, the circadian mechanisms involved are currently unclear. To examine this issue, we constructed models of rapid eye movement sleep deprivation (RSD) and POCD after sevoflurane inhalation, to evaluate the circadian mechanisms underlying preoperative sleep deprivation-induced POCD after sevoflurane inhalation. ⋯ In addition, sevoflurane inhalation activated the plasma expression of S100β and IL-6, particularly after sleep deprivation. Sleep deprivation aggravated pathogenic impairment of pyramidal neurons and activated astrocytes in CA1 after sevoflurane inhalation. These results suggest that preoperative RSD aggravates hippocampal memory impairment by enhancing neuroinflammatory injuries after sevoflurane inhalation, which is related to hippocampal clock gene abnormalities.
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To determine the association between functional connectivity (FC) of functional-segmented anterior and posterior portions of the hippocampus and performance on verbal and visual memory tests in a young, healthy population. ⋯ The present results demonstrated that, the anterior hippocampus was specifically involved in the visual memory processing, whereas the posterior hippocampus contributed to both the verbal and visual memories, which may have implications for a functionally synergetic and dissociable role of the hippocampus in different kinds of memory.
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Autism is a neurodevelopmental disease which is characterized by its core behavioral symptoms such as impairment in social interaction and stereotyped repetitive behavior. Th17 immune responses and oxidative stress are reported to be elevated in both human autistic subjects and BTBR T + Itpr3tf/J (BTBR) mice. On the other hand, activation of nuclear factor erythroid 2 related factor (Nrf2), a master transcription factor is essential for the management of anti-inflammatory and antioxidant genes. ⋯ Furthermore, sulforaphane-treated BTBR and C57 mice had upregulated enzymatic antioxidant defenses in neutrophils/cerebellum (SOD, GPx and GR expression and activity). We reason that activation of Nrf2 by sulforaphane corrected Th17 immune dysfunction and oxidant-antioxidant imbalance in periphery and brain in BTBR mice. These mechanisms lead to improvement in autism-like symptoms in BTBR mice.
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Anorexia by osmotic dehydration is an adaptive response to hypernatremia and hyperosmolaemia induced by ingestion of a hypertonic solution. Dehydration-induced anorexia (DIA) reproduces weight loss and avoidance of food, despite its availability. By using this model, we previously showed increased reactive astrocyte density in the rat dorsal hippocampus, suggesting a pro-inflammatory environment where microglia may play an important role. ⋯ Accordingly, the activated/resting microglia ratio was significantly increased in CA2-CA3 and DG, in DIA and FFR groups. Finally, western blot analysis showed increased expression of IBA1, TNF-α, IL-6 and IL-1β in the hippocampus of both experimental groups. We conclude that anorexia triggers increased reactive microglial density and expression of TNF-α, IL-6 and IL-1β; this environment may result in hippocampal neuroinflammation.
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Drug addiction is a widespread social problem, which not only brings adverse consequences to the human body, but also causes great burden to the society. However, it's still unclear how the long-term and sustained cocaine exposure will affect clock genes' expression in the reward related brain areas. We hypothesize that chronic cocaine exposure causes changes in the circadian rhythmic expression of clock genes in brain regions associated with reward, since previous studies have shown that cocaine use causes circadian disorders. ⋯ A blunting of circadian oscillations of rPer1 expression occurred in the NAc core and shell and hippocampus; of rPer2 expression occurred in the SCN, PFC, NAc core and hippocampus; of rPer3 expression occurred in the SCN, PFC, NAc shell, hippocampus and VTA; of rCry expression occurred in the NAc core and shell, hippocampus and VTA; of rBmal1 expression occurred in the PFC, NAc shell, hippocampus and VTA in cocaine - treated rats. These rhythm changes accompanied by significant increase in rPer1, rPer2, rPer3 and rBmal1 in the PFC, rPer1, rPer2 and rBmal1 in the hippocampus; significant decrease in rPer2, rPer3 and rCry in the SCN, rPer3, rCry, rBmal1 and rClock in the NAc core compared to control rats. rClock expression in cocaine - treated rats showed no rhythmic change, identical to control rats. These results suggest that chronic cocaine exposure results in disturbances in clock genes' expression in reward related areas.