Altered astrocyte calcium homeostasis and proliferation in the Ts65Dn mouse, a model of Down syndrome

被引:16
|
作者
Bambrick, LL
Yarowsky, PJ
Krueger, BK
机构
[1] Univ Maryland, Sch Med, Dept Anesthesiol, Baltimore, MD 21201 USA
[2] Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA
[3] Univ Maryland, Sch Med, Dept Pharmacol & Expt Therapeut, Baltimore, MD 21201 USA
关键词
neurogenesis; trisomy; 16; Ts65Dn; astrocyte; calcium homeostasis;
D O I
10.1002/jnr.10630
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Genes from the Down syndrome (DS) critical region of human chromosome 21, which contribute to the pathology of DS, are also found on mouse chromosome 16. Several animal models of DS with triplication of genes from the DS critical region have been generated, including mouse trisomy 16 (Ts16) and a partial trisomic mouse, Ts65Dn. Using computer-assisted imaging of fura-2 fluorescence, we found an elevation of intracellular cytoplasmic calcium in cortical astrocytes from neonatal Ts65Dn mouse brain, similar to that observed previously in embryonic Ts16 astrocytes. Furthermore, astrocytes from both Ts65Dn and Ts16 cortex fail to respond to the anti-proliferative actions of glutamate. These results suggest that defective regulation of cell proliferation and cellular calcium can result from triplication of DS critical region genes. (C) 2003 Wiley-Liss, Inc.
引用
收藏
页码:89 / 94
页数:6
相关论文
共 50 条
  • [31] Increased hippocampal epigenetic age in the Ts65Dn mouse model of Down Syndrome
    Ravaioli, Francesco
    Stagni, Fiorenza
    Guidi, Sandra
    Pirazzini, Chiara
    Garagnani, Paolo
    Silvani, Alessandro
    Zoccoli, Giovanna
    Bartesaghi, Renata
    Bacalini, Maria Giulia
    FRONTIERS IN AGING NEUROSCIENCE, 2024, 16
  • [32] Alterations of central noradrenergic transmission in Ts65Dn mouse, a model for Down syndrome
    Dierssen, M
    Vallina, IF
    Baamonde, C
    GarciaCalatayud, S
    Lumbreras, MA
    Florez, J
    BRAIN RESEARCH, 1997, 749 (02) : 238 - 244
  • [33] Hippocampal and cerebellar BDNF levels in the Ts65Dn mouse model of Down syndrome
    Roberson, Robin
    Kuddo, Thea
    Caballero, Madeline
    Horowitz, Kari
    Spong, Catherine Y.
    AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 2012, 206 (01) : S320 - S320
  • [34] Synaptic Vesicle Recycling Is Unaffected in the Ts65Dn Mouse Model of Down Syndrome
    Marland, Jamie R. K.
    Smillie, Karen J.
    Cousin, Michael A.
    PLOS ONE, 2016, 11 (01):
  • [35] Quantitative PCR genotyping assay for the Ts65Dn mouse model of Down syndrome
    Liu, DP
    Schmidt, C
    Billings, M
    Davisson, MT
    BIOTECHNIQUES, 2003, 35 (06) : 1170 - +
  • [36] Luteolin induces hippocampal neurogenesis in the Ts65Dn mouse model of Down syndrome
    Wen-Bo Zhou
    Zong-Ning Miao
    Bin Zhang
    Wei Long
    Fang-Xiu Zheng
    Jing Kong
    Bin Yu
    NeuralRegenerationResearch, 2019, 14 (04) : 613 - 620
  • [37] Postnatal lethality and cardiac anomalies in the Ts65Dn Down Syndrome mouse model
    Clara S. Moore
    Mammalian Genome, 2006, 17
  • [38] APP accumulation and inflammation in the Ts65dn mouse, a model for Down's syndrome
    Lockrow, J
    Willis, L
    Granholm, AC
    Sambamurti, K
    EXPERIMENTAL NEUROLOGY, 2006, 198 (02) : 578 - 578
  • [39] Postnatal lethality and cardiac anomalies in the Ts65Dn Down Syndrome mouse model
    Moore, Clara S.
    MAMMALIAN GENOME, 2006, 17 (10) : 1005 - 1012
  • [40] Increased incidence of intermittent hypoxemia in the Ts65Dn mouse model of Down syndrome
    Das, Devsmita
    Medina, Brian
    Baktir, Mehmet Akif
    Mojabi, Fatemeh S.
    Fahimi, Atoossa
    Ponnusamy, Ravikumar
    Salehi, Ahmad
    NEUROSCIENCE LETTERS, 2015, 604 : 91 - 96