Impairment of short term memory in rats with hepatic encephalopathy due to bile duct ligation

被引:0
作者
Renata Leke
Diogo L. Oliveira
Luiz F. Forgiarini
Thayssa D. C. Escobar
Thais O. Hammes
Fabíola S. Meyer
Susanne Keiding
Themis R. Silveira
Arne Schousboe
机构
[1] Research Center of Hospital de Clínicas de Porto Alegre,Experimental Hepatology and Gastroenterology Laboratory
[2] Federal University of Rio Grande do Sul,Post
[3] Federal University of Rio Grande do Sul,Graduation in Child and Adolescents Health
[4] University of Copenhagen,Department of Biochemistry
[5] Aarhus University Hospital,Department of Drug Design and Pharmacology
[6] Aarhus University Hospital,Positron Emission Tomography Centre
来源
Metabolic Brain Disease | 2013年 / 28卷
关键词
Hepatic encephalopathy; Bile duct-ligated rats; Short term memory; Long term memory; Object recognition;
D O I
暂无
中图分类号
学科分类号
摘要
Hepatic encephalopathy (HE) arises from acute or chronic liver diseases and leads to cognitive deficits. Different animal models for the study of HE have demonstrated learning and memory impairment and a number of neurotransmitter systems have been proposed to be involved in this. Recently, it was described that bile duct-ligated (BDL) rats exhibited altered spatio-temporal locomotor and exploratory activities and biosynthesis of neurotransmitter GABA in brain cortices. Therefore, the aim of this study was to evaluate cognition in the same animal model. Male adult Wistar rats underwent common bile duct ligation (BDL rats) or manipulation of common bile duct without ligation (control rats). Six weeks after surgery, control and BDL rats underwent object recognition behavioral task. The BDL rats developed chronic liver failure and exhibited a decreased discrimination index for short term memory (STM) when compared to the control group. There was no difference in long term memory (LTM) as well as in total time of exploration in the training, STM and LTM sessions between the BDL and control rats. Therefore, the BDL rats demonstrated impaired STM for recognition memory, which was not due to decreased exploration.
引用
收藏
页码:187 / 192
页数:5
相关论文
共 169 条
  • [1] Ahboucha S(2007)The neurosteroid system: an emerging therapeutic target for hepatic encephalopathy Metab Brain Dis 22 291-308
  • [2] Butterworth RF(2008)Indomethacin improves locomotor deficit and reduces brain concentrations of neuroinhibitory steroids in rats following portacaval anastomosis Neurogastroenterol Motil 20 949-57
  • [3] Ahboucha S(2012)Reduced brain levels of DHEAS in hepatic coma patients: Significance for increased GABAergic tone in hepatic encephalopathy Neurochem Int 61 48-53
  • [4] Jiang W(1999)Hepatic encephalopathy: molecular mechanisms underlying the clinical syndrome J Neurol Sci. 170 138-46
  • [5] Chatauret N(2000)Effect of ammonia on GABA uptake and release in cultured astrocytes Neurochem Int 36 389-95
  • [6] Mamer O(2006)Object recognition in rats and mice: a one-trial non-matching-to-sample learning task to study “recognition memory” Nat Protoc 1 1306-11
  • [7] Baker GB(2007)Motor activity is modulated via different neuronal circuits in rats with chronic liver failure than in normal rats Eur J Neurosci 25 2112-22
  • [8] Butterworth RF(2007)Inflammation and hepatic encephalopathy: ibuprofen restores learning ability in rats with portacaval shunts Hepatology 46 514-9
  • [9] Ahboucha S(2009)Hyperammonemia increases GABAergic tone in the cerebellum but decreases it in the rat cortex Gastroenterology 136 1359-67
  • [10] Talani G(2005)Restoration of learning ability in hyperammonemic rats by increasing extracellular cGMP in brain Brain Res 1036 115-21