Surgery-induced behavioral changes in aged rats

Hovens, Iris B.; Schoemaker, Regien G.; Zee, Eddy A. van der; Heineman, Erik; Nyakas, Csaba; Leeuwen, Barbara L. van

doi:10.1016/j.exger.2013.07.011

Cited by 60 publications

(82 citation statements)

References 59 publications

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“…Various animal models of POCD have demonstrated elevations in pro-inflammatory cytokines and other proinflammatory mediators in the hippocampus (Cibelli et al, 2010; Barrientos et al, 2012; Terrando et al, 2013; Hovens et al, 2014a,b; Zhang et al, 2014). We, and others, have shown that hippocampal memory function was significantly more impaired by surgery in aged animals compared to younger control animals (Barrientos et al, 2012; Hovens et al, 2013, 2014b; Li et al, 2014; Sun et al, 2014; Yu et al, 2014). This pattern has been found following a variety of surgical procedures including exploratory abdominal surgery (Barrientos et al, 2012; Hovens et al, 2014b; Li et al, 2014), stabilized tibial fracture surgery (Sun et al, 2014), and partial hepatectomy (Li et al, 2013).…”

Section: Introductionmentioning

confidence: 57%

Neuroinflammation in the normal aging hippocampus

et al. 2015

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A consequence of normal aging is a greater susceptibility to memory impairments following an immune challenge such as infection, surgery, or traumatic brain injury. The neuroinflammatory response, produced by these challenges results in increased and prolonged production of pro-inflammatory cytokines in the otherwise healthy aged brain. Here we discuss the mechanisms by which long-lasting elevations in pro-inflammatory cytokines in the hippocampus produce memory impairments. Sensitized microglia are a primary source of this exaggerated neuroinflammatory response and appear to be a hallmark of the normal aging brain. We review the current understanding of the causes and effects of normal aging-induced microglial sensitization, including dysregulations of the neuroendocrine system, potentiation of neuroinflammatory responses following an immune challenge, and the impairment of memories. We end with a discussion of therapeutic approaches to prevent these deleterious effects.

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Section: Introductionmentioning

confidence: 57%

Neuroinflammation in the normal aging hippocampus

et al. 2015

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“…Recent studies have drawn a conclusion that anesthesia alone for a period comparable to the duration of the surgical procedure does not induce cognitive deficits in animals (Cao et al, 2012;Chen et al, 2013;Hovens et al, 2013Hovens et al, , 2014, thus we did not include the mice receiving anesthesia alone in the study protocol. However, we could not exclude the influence of anesthesia on microglial activation and neuroinflammation in the present study.…”

Section: Discussionmentioning

confidence: 99%

NADPH oxidase 2-derived reactive oxygen species in the hippocampus might contribute to microglial activation in postoperative cognitive dysfunction in aged mice

Zhang

et al. 2016

Brain, Behavior, and Immunity

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“…Many published studies also used OFT to reflect the changes in the hippocampus. 28,29) The mobility score showed an ability of locomotion. The latency to leave the center is an indication of anxiety.…”

Section: Discussionmentioning

confidence: 99%

Prevention of Postoperative Fatigue Syndrome in Rat Model by Ginsenoside Rb1 <i>via</i> Down-Regulation of Inflammation along the NMDA Receptor Pathway in the Hippocampus

Chen

Liu

Chen

et al. 2015

Biological & Pharmaceutical Bulletin

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Postoperative fatigue syndrome (POFS) is a common complication which decelerates recovery after surgery. The present study investigated the anti-fatigue effect of ginsenoside Rb1 (GRb1) through the inflammatory cytokine-mediated N-methyl-D-aspartate (NMDA) receptor pathway. A POFS rat model was created by major small intestinal resection and assessed with an open field test. Real-time quantitative polymerase chain reaction, western blot analysis, high performance liquid chromatography and a transmission electron microscopic analysis were used to determine typical biochemical parameters in the hippocampus. Our results showed that POFS rats exhibited fatigue associated with an increased expression of inflammatory cytokines and NMDA receptor 1, higher (kynurenine)/(tryptophan) and (kynurenine)/(kynurenic acid) on postoperative days 1 and 3, and an increased expression of indoleamine 2,3-dioxygenase (IDO) on postoperative day 1. Degenerated neurons were found in the hippocampus of POFS rats. The NMDA receptor antagonist MK801 had a significant effect on central fatigue on postoperative day 1. GRb1 had no effect on IDO or tryptophan metabolism, but exhibited a significant effect on POFS by inhibiting the expression of inflammatory cytokines and NMDA receptor 1. These data suggested that inflammatory cytokines could activate tryptophan metabolism to cause POFS through the NMDA receptor pathway. GRb1 had an anti-fatigue effect on POFS by reducing inflammatory cytokines and NMDA receptors.

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Surgery-induced behavioral changes in aged rats

Cited by 60 publications

References 59 publications

Neuroinflammation in the normal aging hippocampus

Neuroinflammation in the normal aging hippocampus

NADPH oxidase 2-derived reactive oxygen species in the hippocampus might contribute to microglial activation in postoperative cognitive dysfunction in aged mice

Prevention of Postoperative Fatigue Syndrome in Rat Model by Ginsenoside Rb1 <i>via</i> Down-Regulation of Inflammation along the NMDA Receptor Pathway in the Hippocampus

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