Document Detail


Protective effects of lithium treatment for spatial memory deficits induced by tau hyperphosphorylation in splenectomized rats.
MedLine Citation:
PMID:  20659131     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
1. Postoperative cognitive dysfunction has become more prevalent in recent years. We used a splenectomized rat model with postoperative spatial learning and memory deficits to investigate the role of tau hyperphosphorylation and glycogen synthase kinase-3β (GSK-3β) within the hippocampus. 2. Cognitive function was assessed in a Y-maze 1 day before and 1, 3 and 7 days after surgery. We measured site-specific phosphorylation of hippocampal tau (Thr-205 and Ser-396), GSK-3β activity and expression of interleukin-1β (IL-1β), tumour necrosis factor-α (TNF-α) mRNA and protein as markers of inflammation. We also tested the effects of treatment with lithium chloride (LiCl), a GSK-3β inhibitor. 3. Splenectomy was associated with learning and memory impairment 3 days later, as well as a rapid and massive hyperphosphorylation of hippocampal tau at Thr-205 and Ser-396, activated GSK-3β, and increased IL-1β and TNF-α expression. LiCl completely restored tau hyperphosphorylation to control levels. 4. These data from the splenectomized rat model suggest that inflammatory factors affect tau pathology through the GSK-3β signalling pathway and that LiCl is a promising treatment for postoperative cognitive deficits.
Authors:
Wen-Fei Tan; Xue-Zhao Cao; Jun-Ke Wang; Huang-Wei Lv; Bin-Yang Wu; Hong Ma
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical and experimental pharmacology & physiology     Volume:  37     ISSN:  1440-1681     ISO Abbreviation:  Clin. Exp. Pharmacol. Physiol.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-29     Completed Date:  2011-09-02     Revised Date:  2011-11-02    
Medline Journal Info:
Nlm Unique ID:  0425076     Medline TA:  Clin Exp Pharmacol Physiol     Country:  Australia    
Other Details:
Languages:  eng     Pagination:  1010-5     Citation Subset:  IM    
Copyright Information:
© 2010 The Authors. Clinical and Experimental Pharmacology and Physiology © 2010 Blackwell Publishing Asia Pty Ltd.
Affiliation:
Department of Anaesthesiology, First Hospital of China Medical University, Shenyang, China.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Biological Markers / metabolism
Glycogen Synthase Kinase 3 / antagonists & inhibitors,  physiology
Inflammation Mediators / metabolism,  therapeutic use
Lithium Chloride / therapeutic use*
Male
Maze Learning / drug effects,  physiology
Memory Disorders / metabolism*,  pathology,  prevention & control*
Neuroprotective Agents / therapeutic use*
Phosphorylation / drug effects,  physiology
Postoperative Complications / metabolism,  pathology,  prevention & control*
Rats
Rats, Sprague-Dawley
Signal Transduction / drug effects,  physiology
Splenectomy / adverse effects*
Treatment Outcome
tau Proteins / metabolism*,  physiology
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Inflammation Mediators; 0/Neuroprotective Agents; 0/tau Proteins; 7447-41-8/Lithium Chloride; EC 2.7.11.1/glycogen synthase kinase 3 beta; EC 2.7.11.26/Glycogen Synthase Kinase 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Nitric oxide induced sinusoidal relaxation after a propranolol priming dose in the perfused rat live...
Next Document:  Coronary vascular dysfunction promoted by oxidative-nitrative stress in SHRSP.Z-Lepr(fa) /IzmDmcr ra...