Linked Life Data

15590143

Source:http://linkedlifedata.com/resource/pubmed/id/15590143

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-12-13
pubmed:abstractText
Various types of learning, including operant conditioning, induce an increase in cellular activation concomitant with an increase in local cerebral glucose utilization (LCGU). This increase is mediated by increased cerebral blood flow or changes in brain capillary density and diameter. Because glucose transporters are ultimately responsible for glucose uptake, we examined their plastic expression in response to cellular activation. In vitro and in vivo studies have demonstrated that cerebral glucose transporter 1 (GLUT1) expression consistently parallels changes in LCGU. The present study is the first to investigate the effect of memory processing on glucose transporters expression. Changes in GLUT expression produced by training in an operant conditioning task were measured in the brain of CD1 mice. Using semi-quantitative immunohistochemistry, Western blot and real time RT-PCR the cerebral GLUT1 and GLUT3 expression was quantified immediately, 220 min and 24 h following training. Relative to sham-trained and naive controls, operant conditioning training induced an immediate increase in GLUT1 immunoreactivity level in the hippocampus CA1 pyramidal cells as well as in the sensorimotor cortex. At longer post-learning delays, GLUT1 immunoreactivity decreased in the sensorimotor cortex and putamen. Parallel to the changes in protein levels, hippocampus GLUT1 mRNA level also increased immediately following learning. No effect of learning was found on hippocampal GLUT3 protein or mRNA expression. Measures of changes in glucose transporters expression present a link between cellular activation and glucose metabolism. The learning-induced localized increases in GLUT1 protein as well as mRNA levels observed in the present study confirm the previous findings that GLUT1 expression is plastic and respond to changes in cellular metabolic demands.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
130
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
591-600
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15590143-Animals, pubmed-meshheading:15590143-Blotting, Western, pubmed-meshheading:15590143-Brain Chemistry, pubmed-meshheading:15590143-Conditioning, Operant, pubmed-meshheading:15590143-Data Interpretation, Statistical, pubmed-meshheading:15590143-Fluorescent Antibody Technique, pubmed-meshheading:15590143-Glucose, pubmed-meshheading:15590143-Glucose Transporter Type 1, pubmed-meshheading:15590143-Glucose Transporter Type 3, pubmed-meshheading:15590143-Immunohistochemistry, pubmed-meshheading:15590143-Male, pubmed-meshheading:15590143-Memory, pubmed-meshheading:15590143-Mice, pubmed-meshheading:15590143-Monosaccharide Transport Proteins, pubmed-meshheading:15590143-Nerve Tissue Proteins, pubmed-meshheading:15590143-Neuronal Plasticity, pubmed-meshheading:15590143-Pyramidal Cells, pubmed-meshheading:15590143-RNA, pubmed-meshheading:15590143-Reverse Transcriptase Polymerase Chain Reaction
pubmed:year
2005
pubmed:articleTitle
Glucose transporter plasticity during memory processing.
pubmed:affiliation
School of Psychology, University of Ottawa, 11 Marie Curie, Room 215, Ottawa, Ontario, Canada K1N 6N5.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't