首页> 外文期刊>Physiology & behavior >Cognitive impairment and gene expression alterations in a rodent model of binge eating disorder
【24h】

Cognitive impairment and gene expression alterations in a rodent model of binge eating disorder

机译:狂暴紊乱啮齿动物模型中的认知障碍与基因表达改变

获取原文
获取原文并翻译 | 示例
获取外文期刊封面目录资料

摘要

Abstract Binge eating disorder (BED) is defined as recurrent, distressing over-consumption of palatable food (PF) in a short time period. Clinical studies suggest that individuals with BED may have impairments in cognitive processes, executive functioning, impulse control, and decision-making, which may play a role in sustaining binge eating behavior. These clinical reports, however, are limited and often conflicting. In this study, we used a limited access rat model of binge-like behavior in order to further explore the effects of binge eating on cognition. In binge eating prone (BEP) rats, we found novel object recognition (NOR) as well as Barnes maze reversal learning (BM-RL) deficits. Aberrant gene expression of brain derived neurotrophic factor ( Bdnf ) and tropomyosin receptor kinase B ( TrkB ) in the hippocampus (HPC)-prefrontal cortex (PFC) network was observed in BEP rats. Additionally, the NOR deficits were correlated with reductions in the expression of TrkB and insulin receptor ( Ir ) in the CA3 region of the hippocampus. Furthermore, up-regulation of serotonin-2C ( 5-HT 2C ) receptors in the orbitoprefrontal cortex (OFC) was associated with BM-RL deficit. Finally, in the nucleus accumbens (NAc), we found decreased dopamine receptor 2 ( Drd2 ) expression among BEP rats. Taken together, these data suggest that binge eating vegetable shortening may induce contextual and reversal learning deficits which may be mediated, at least in part, by the altered expression of genes in the CA3-OFC-NAc neural network. Highlights ? This study employed a rodent model to examine the effects of high-fat binge eating on cognitive performances. ? Binge eating prone (BEP) rats were impaired in contextual learning and spatial reversal learning. ? BEP rats were found to have disrupted Bdnf-TrkB expression in the hippocampal and prefrontal cortex sub-regions. ? Altered expression of serotonin-2C receptor and dopamine 1 and 4 receptors in orbitofrontal cortex was found in BEP rats. ? Binge eating behavior was related to the decreases in the dopamine 2 receptor expression in the nucleus accumbens region.
机译:摘要狂犬病患者(床)被定义为复发,在短时间内令人痛苦的可口食品(PF)。临床研究表明,床上的个体可能在认知过程中具有损伤,执行功能,脉冲控制和决策,这可能在维持狂暴饮食行为方面发挥作用。然而,这些临床报告是有限的,通常是矛盾的。在这项研究中,我们使用了有限的狂欢行为的访问大鼠模型,以进一步探索狂犬病对认知的影响。在狂犬病的易于(BEP)大鼠中,我们发现了新的对象识别(也不)以及Barnes迷宫逆转学习(BM-RL)赤字。在BEP大鼠中观察到海马(HPC) - 预级皮质(PFC)网络中脑衍生的神经营养因子(BDNF)和对吡喃素受体激酶B(TRKB)的异常基因表达。另外,与海马CA3区的TRKB和胰岛素受体(IR)表达的降低相关,也与缺陷相关。此外,在镁酞普罗伦特皮质皮质(OFC)中的血清素-2C(5-HT 2C)受体的上调与BM-RL缺陷有关。最后,在核常规(NAC)中,我们发现BEP大鼠中的多巴胺受体2(DRD2)表达降低。这些数据表明,狂犬病患者缩短可能诱导至少部分地通过CA3-OF-NAC神经网络中的基因表达的改变的基因表达来介导的上下文和逆转学习缺陷。强调 ?本研究采用啮齿动物模型来检查高脂狂犬病对认知性能的影响。还在语境学习和空间逆转学习中,狂犬病般的易患(BEP)大鼠受损。还发现BEP大鼠在海马和前额叶皮质子区域中破坏了BDNF-TRKB表达。还在BEP大鼠中发现了在BEP大鼠中发现了羟色胺-2C受体和多巴胺1和4个受体的改变的胰腺皮质中的表达。还血迹吃行为与细胞核骨胎区中多巴胺2受体表达的减少有关。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号