Cell Lines Derived from Hippocampal Neurons of the Normal and Trisomy 16 Mouse Fetus (a Model for Down Syndrome) Exhibit Neuronal Markers, Cholinergic Function, and Functional Neurotransmitter Receptors

2002 ◽  
Vol 177 (1) ◽  
pp. 159-170 ◽  
Author(s):  
A Cárdenas
Keyword(s):  
Down Syndrome ◽  
Cell Lines ◽  
Hippocampal Neurons ◽  
Neurotransmitter Receptors ◽  
Mouse Fetus ◽  
Trisomy 16 ◽  
Neuronal Markers ◽  
Cholinergic Function

Knockdown of amyloid precursor protein normalizes cholinergic function in a cell line derived from the cerebral cortex of a trisomy 16 mouse: An animal model of down syndrome

2006 ◽  
Vol 84 (6) ◽  
pp. 1303-1310 ◽  
Author(s):  
Patricia Opazo ◽  
Katherine Saud ◽  
Michelle de Saint Pierre ◽  
Ana María Cárdenas ◽  
David D. Allen ◽  
...  
Keyword(s):  
Animal Model ◽  
Down Syndrome ◽  
Cerebral Cortex ◽  
Amyloid Precursor Protein ◽  
Cell Line ◽  
Precursor Protein ◽  
Trisomy 16 ◽  
Cholinergic Function ◽  
A Cell

Regional alteration of cholinergic function in central neurons of trisomy 16 mouse fetuses, an animal model of human trisomy 21 (Down syndrome)

1994 ◽  
Vol 658 (1-2) ◽  
pp. 27-32 ◽  
Author(s):  
J.L. Fiedler ◽  
C.J. Epstein ◽  
S.I. Rapoport ◽  
R. Caviedes ◽  
P. Caviedes
Keyword(s):  
Animal Model ◽  
Down Syndrome ◽  
Trisomy 21 ◽  
Trisomy 16 ◽  
Cholinergic Function ◽  
Central Neurons ◽  
Mouse Fetuses

Establishment and characterization of immortalized neuronal cell lines derived from the spinal cord of normal and trisomy 16 fetal mice, an animal model of Down syndrome

2002 ◽  
Vol 68 (1) ◽  
pp. 46-58 ◽  
Author(s):  
Ana María Cárdenas ◽  
David D. Allen ◽  
Christian Arriagada ◽  
Alexis Olivares ◽  
Lori B. Bennett ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Animal Model ◽  
Down Syndrome ◽  
Cell Lines ◽  
Neuronal Cell ◽  
Trisomy 16 ◽  
Fetal Mice ◽  
Neuronal Cell Lines

Impaired cholinergic function in cell lines derived from the cerebral cortex of normal and trisomy 16 mice

2000 ◽  
Vol 12 (9) ◽  
pp. 3259-3264 ◽  
Author(s):  
David D. Allen ◽  
José Martín ◽  
Christian Arriagada ◽  
Ana María Cárdenas ◽  
Stanley I. Rapoport ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Cell Lines ◽  
Trisomy 16 ◽  
Cholinergic Function

Glutamate-Promoted Survival in Hippocampal Neurons: A Defect in Mouse Trisomy 16

1996 ◽  
pp. 133-139
Author(s):  
Linda L. Bambrick ◽  
Paul J. Yarowsky ◽  
Bruce K. Krueger
Keyword(s):  
Hippocampal Neurons ◽  
Trisomy 16

scholarly journals Consequences of Trisomy 16 for Mouse Brain Development: Corticogenesis in a Model of Down Syndrome

1996 ◽  
Vol 16 (19) ◽  
pp. 6175-6182 ◽  
Author(s):  
Tarik F. Haydar ◽  
Mary E. Blue ◽  
Mark E. Molliver ◽  
Bruce K. Krueger ◽  
Paul J. Yarowsky
Keyword(s):  
Down Syndrome ◽  
Brain Development ◽  
Mouse Brain ◽  
Trisomy 16 ◽  
Mouse Brain Development

Ts65Dn, a Mouse Model of Down Syndrome, Exhibits Increased GABAB-Induced Potassium Current

2007 ◽  
Vol 97 (1) ◽  
pp. 892-900 ◽  
Author(s):  
Tyler K. Best ◽  
Richard J. Siarey ◽  
Zygmunt Galdzicki
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Hippocampal Neurons ◽  
Single Channel ◽  
Extra Chromosome ◽  
Functional Expression ◽  
Chromosome 21 ◽  
Fluctuation Analysis ◽  
Response Curves ◽  
Girk Channel

Down syndrome (DS) is the most common nonheritable cause of mental retardation. DS is the result of the presence of an extra chromosome 21 and its phenotype may be a consequence of overexpressed genes from that chromosome. One such gene is Kcnj6/Girk2, which encodes the G-protein-coupled inward rectifying potassium channel subunit 2 (GIRK2). We have recently shown that the DS mouse model, Ts65Dn, overexpresses GIRK2 throughout the brain and in particular the hippocampus. Here we report that this overexpression leads to a significant increase (∼2-fold) in GABAB-mediated GIRK current in primary cultured hippocampal neurons. The dose response curves for peak and steady-state GIRK current density is significantly shifted left toward lower concentrations of baclofen in Ts65Dn neurons compared with diploid controls, consistent with increased functional expression of GIRK channels. Stationary fluctuation analysis of baclofen-induced GIRK current from Ts65Dn neurons indicated no significant change in single-channel conductance compared with diploid. However, significant increases in GIRK channel density was found in Ts65Dn neurons. In normalized baclofen-induced GIRK current and GIRK current kinetics no difference was found between diploid and Ts65Dn neurons, which suggests unimpaired mechanisms of interaction between GIRK channel and GABAB receptor. These results indicate that increased expression of GIRK2 containing channels have functional consequences that likely affect the balance between excitatory and inhibitory neuronal transmission.

Sign in / Sign up

Export Citation Format

Share Document