The effects of aging and genotype on NMDA receptor expression in growth hormone receptor knockout (GHRKO) mice

Caloric restriction enhances N-methyl-D-aspartate (NMDA) receptor binding and upregulates messenger RNA expression of the GluN1 subunit during aging. Old growth hormone receptor knockout mice resemble old calorically restricted rodents in enhanced life span and brain function, as compared with aged...

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Bibliographic Details
Published in:The journals of gerontology. Series A, Biological sciences and medical sciences Biological sciences and medical sciences, 2011-06, Vol.66 (6), p.607-619
Main Authors: Magnusson, Kathy Ruth, Das, Siba Ranjan, Kronemann, Daniel, Bartke, Andrzej, Patrylo, Peter R
Format: Article
Language:English
Subjects:
Aging
Aging - metabolism
Animals
Gene expression
Genotype
Genotype & phenotype
Glutamic Acid - metabolism
Growth hormones
Journal of Gerontology: BIOLOGICAL SCIENCES
Male
Mice
Mice, Inbred Strains
Mice, Knockout
Receptors, N-Methyl-D-Aspartate - analysis
Receptors, N-Methyl-D-Aspartate - genetics
Receptors, N-Methyl-D-Aspartate - metabolism
Receptors, Somatotropin - genetics
Receptors, Somatotropin - physiology
RNA, Messenger - analysis
Rodents
Studies
T cell receptors
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Summary:Caloric restriction enhances N-methyl-D-aspartate (NMDA) receptor binding and upregulates messenger RNA expression of the GluN1 subunit during aging. Old growth hormone receptor knockout mice resemble old calorically restricted rodents in enhanced life span and brain function, as compared with aged controls. This study examined whether aged growth hormone receptor knockout mice also show enhanced expression of NMDA receptors. Six or 23- to 24-month-old male normal-sized control or dwarf growth hormone receptor knockout mice were assayed for NMDA-displaceable [(3)H]glutamate binding (autoradiography) and GluN1 subunit messenger RNA (in situ hybridization). There was slight sparing of NMDA receptor binding densities within aged medial prefrontal and motor cortices, similar to caloric restriction, but there were greater age-related declines in GluN1 messenger RNA in growth hormone receptor knockout versus control mice. These results suggest that some of the functional improvements in aged mice with altered growth hormone signaling may be due to enhancement of NMDA receptors, but not through the upregulation of messenger RNA for the GluN1 subunit.
ISSN:1079-5006
1758-535X
DOI:10.1093/gerona/glr024