Robin Roberson1, Laura Toso, Daniel Abebe, Catherine Y Spong. 1. Unit on Perinatal and Developmental Neurobiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20895, USA. robersor@mail.nih.gov
Abstract
OBJECTIVE: Down syndrome (DS), a major cause of mental retardation, affects 1 of 800 newborns. Mouse models for Down syndrome have been studied and found to have developmental and learning deficits, including the Ts65Dn (DS) mouse model. N-methyl-D-aspartate receptor NR2B subunit enhances synaptic plasticity. The up-regulation of KIF17, a motor protein that transports NR2B to the synaptic region parallels up-regulation of synaptic NR2B. Down regulation of KIF17 reflects up-regulation of less plastic NR2A subunit. We evaluated NR2B, NR2A, and KIF17 in Ts65Dn and control mice. STUDY DESIGN: Ts65Dn (4) and control (4) adult brains were collected; NR2A, NR2B, and KIF17 were measured by Western blot and quantified using National Institutes of Health Image software. Comparisons were made using analysis of variance, < .05 was considered significant. RESULTS: There was a significant decrease in KIF17 (P = .04) level in Ts65Dn mice as compared with the control animals, but there were no significant differences in the levels of NR2A (P = .79) and NR2B (P = .96). CONCLUSION: The significant decrease of KIF17 inTs65Dn animals may in part mediate cognitive defects in DS.
OBJECTIVE: Down syndrome (DS), a major cause of mental retardation, affects 1 of 800 newborns. Mouse models for Down syndrome have been studied and found to have developmental and learning deficits, including the Ts65Dn (DS) mouse model. N-methyl-D-aspartate receptor NR2B subunit enhances synaptic plasticity. The up-regulation of KIF17, a motor protein that transports NR2B to the synaptic region parallels up-regulation of synaptic NR2B. Down regulation of KIF17 reflects up-regulation of less plastic NR2A subunit. We evaluated NR2B, NR2A, and KIF17 in Ts65Dn and control mice. STUDY DESIGN:Ts65Dn (4) and control (4) adult brains were collected; NR2A, NR2B, and KIF17 were measured by Western blot and quantified using National Institutes of Health Image software. Comparisons were made using analysis of variance, < .05 was considered significant. RESULTS: There was a significant decrease in KIF17 (P = .04) level in Ts65Dnmice as compared with the control animals, but there were no significant differences in the levels of NR2A (P = .79) and NR2B (P = .96). CONCLUSION: The significant decrease of KIF17 inTs65Dn animals may in part mediate cognitive defects in DS.
Authors: Guido N Vacano; David S Gibson; Abdullah Arif Turjoman; Jeremy W Gawryluk; Jonathan D Geiger; Mark Duncan; David Patterson Journal: Neurobiol Aging Date: 2017-11-26 Impact factor: 4.673
Authors: Sarah M Neuner; Benjamin P Garfinkel; Lynda A Wilmott; Bogna M Ignatowska-Jankowska; Ami Citri; Joseph Orly; Lu Lu; Rupert W Overall; Megan K Mulligan; Gerd Kempermann; Robert W Williams; Kristen M S O'Connell; Catherine C Kaczorowski Journal: Neurobiol Aging Date: 2016-06-17 Impact factor: 4.673
Authors: Jessica H Hall; Frances K Wiseman; Elizabeth M C Fisher; Victor L J Tybulewicz; John L Harwood; Mark A Good Journal: Neurobiol Learn Mem Date: 2016-02-08 Impact factor: 2.877