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Publication : Astrocytic β2 Adrenergic Receptor Gene Deletion Affects Memory in Aged Mice.

First Author  Jensen CJ Year  2016
Journal  PLoS One Volume  11
Issue  10 Pages  e0164721
PubMed ID  27776147 Mgi Jnum  J:252541
Mgi Id  MGI:6100510 Doi  10.1371/journal.pone.0164721
Citation  Jensen CJ, et al. (2016) Astrocytic beta2 Adrenergic Receptor Gene Deletion Affects Memory in Aged Mice. PLoS One 11(10):e0164721
abstractText  In vitro and in vivo studies suggest that the astrocytic adrenergic signalling enhances glycogenolysis which provides energy to be transported to nearby cells and in the form of lactate. This energy source is important for motor and cognitive functioning. While it is suspected that the beta2-adrenergic receptor on astrocytes might contribute to this energy balance, it has not yet been shown conclusively in vivo. Inducible astrocyte specific beta2-adrenergic receptor knock-out mice were generated by crossing homozygous beta2-adrenergic receptor floxed mice (Adrb2flox) and mice with heterozygous tamoxifen-inducible Cre recombinase-expression driven by the astrocyte specific L-glutamate/L-aspartate transporter promoter (GLAST-CreERT2). Assessments using the modified SHIRPA (SmithKline/Harwell/Imperial College/Royal Hospital/Phenotype Assessment) test battery, swimming ability test, and accelerating rotarod test, performed at 1, 2 and 4 weeks, 6 and 12 months after tamoxifen (or vehicle) administration did not reveal any differences in physical health or motor functions between the knock-out mice and controls. However deficits were found in the cognitive ability of aged, but not young adult mice, reflected in impaired learning in the Morris Water Maze. Similarly, long-term potentiation (LTP) was impaired in hippocampal brain slices of aged knock-out mice maintained in low glucose media. Using microdialysis in cerebellar white matter we found no significant differences in extracellular lactate or glucose between the young adult knock-out mice and controls, although trends were detected. Our results suggest that beta2-adrenergic receptor expression on astrocytes in mice may be important for maintaining cognitive health at advanced age, but is dispensable for motor function.
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