Ischemic tolerance resulting from preconditioning ischemia is a neuroprotective mechanism. In cultured astrocytes, its development depends on regulation of the expression of glucose transporter 3 (GLUT3) by the stress sensor/effector AMP-activated protein kinase (AMPK). Here we demonstrate that GLUT3 is upregulated during preconditioning and then downregulated during recovery. We also found that, although AMPK inhibition during preconditioning initially suppressed the upregulation of GLUT3 as shown previously, this was followed by a period of GLUT3 upregulation, enhanced glycogen accumulation, and enhanced tolerance to a subsequent ischemic challenge. These results reveal that AMPK has a complex influence on ischemic tolerance.
Pharmacology, Toxicology and Pharmaceutical Science
2
13%
Biochemistry, Genetics and Molecular Biology
1
7%
Sports and Recreations
1
7%
Other
0
0%
Unknown
2
13%
Attention Score in Context
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 09 June 2015.
All research outputs
#20,655,488
of 25,373,627 outputs
Outputs from Neuroscience Research
#931
of 1,220 outputs
Outputs of similar age
#178,065
of 241,902 outputs
Outputs of similar age from Neuroscience Research
#9
of 10 outputs
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