Document Detail


Cerebral glucose transporters expression and spatial learning in the K-ATP Kir6.2(-/-) knockout mice.
MedLine Citation:
PMID:  16797737     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
K-ATP channels formed of the Sur and Kir subunits are widely distributed in the brain. Sur1-Kir6.2 is the most common combination of K-ATP channel subunits in the brain and Kir6.2 plays an important role in glucose metabolism through pancreatic insulin secretion or hypothalamic glucose sensing. K-ATP channels have also been reported to play a role in memory processing. Therefore, the aim of the present experiment is to assess the gene and protein expression of GLUT1, GLUT3 and GLUT4 in various brain regions of Kir6.2(-/-) K-ATP knockout mice and to test their working memory performance. GLUT4 was measured using two antibodies, one recognizing an intracellular epitope and the other, an extracellular epitope. Relative to their corresponding wild type, semi-quantitative immunohistochemistry showed that GLUT4 protein expression as measured by a GLUT4 antibody recognizing an extracellular epitope was increased in the Kir6.2(-/-) K-ATP mice. However, there was only a small increase in GLUT4 labeling using the GLUT4 antibody recognizing the intracellular epitope. These results suggest a compensatory higher GLUT4 inclusion at the cellular neuronal membrane in the cerebral cortex, hippocampus and cerebellum of the Kir6.2(-/-) K-ATP knockout mice. However, there was no change in GLUT4 gene expression assessed by TaqMan PCR except for a decrease in the cerebellum of these mice. Working memory performance of the Kir6.2(-/-) K-ATP mice was disrupted at age of 12 weeks but not at 5 weeks. The mild glucose intolerance that is observed in the Kir6.2 knockout mice is unlikely to have created the memory deficits observed. Rather, in light of the effects of K-ATP channel modulators on memory, the memory deficits in the Kir6.2(-/-) K-ATP mice are more likely due to the absence of the Kir6.2 and possible disruption of the GLUT4 activity in the brain.
Authors:
C Choeiri; W A Staines; T Miki; S Seino; J-M Renaud; K Teutenberg; C Messier
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-06-23
Journal Detail:
Title:  Behavioural brain research     Volume:  172     ISSN:  0166-4328     ISO Abbreviation:  Behav. Brain Res.     Publication Date:  2006 Sep 
Date Detail:
Created Date:  2006-08-07     Completed Date:  2006-12-28     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8004872     Medline TA:  Behav Brain Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  233-9     Citation Subset:  IM    
Affiliation:
Psychology Faculty, Fresno Pacific University, 1717 South Chestnut Ave. Fresno, CA 93702, USA.
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MeSH Terms
Descriptor/Qualifier:
Age Factors
Analysis of Variance
Animals
Cerebellum / metabolism
Cerebral Cortex / metabolism*
Exploratory Behavior / physiology*
Female
Gene Expression Regulation
Glucose Transporter Type 1 / metabolism
Glucose Transporter Type 3 / metabolism
Glucose Transporter Type 4 / metabolism*
Hippocampus / metabolism
Immunohistochemistry
Male
Maze Learning / physiology*
Memory / physiology
Mice
Mice, Inbred C57BL
Mice, Knockout
Potassium Channels, Inwardly Rectifying / genetics,  metabolism*
RNA, Messenger / analysis
Tissue Distribution
Chemical
Reg. No./Substance:
0/Glucose Transporter Type 1; 0/Glucose Transporter Type 3; 0/Glucose Transporter Type 4; 0/Kir6.2 channel; 0/Potassium Channels, Inwardly Rectifying; 0/RNA, Messenger

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


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