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Publication : Altered long-term potentiation in the young and old Ts65Dn mouse, a model for Down Syndrome.

First Author  Siarey RJ Year  1997
Journal  Neuropharmacology Volume  36
Issue  11-12 Pages  1549-54
PubMed ID  9517425 Mgi Jnum  J:174279
Mgi Id  MGI:5056182 Doi  10.1016/s0028-3908(97)00157-3
Citation  Siarey RJ, et al. (1997) Altered long-term potentiation in the young and old Ts65Dn mouse, a model for Down Syndrome. Neuropharmacology 36(11-12):1549-54
abstractText  We investigated the phenomenon of long-term potentiation (LTP) in a genetic model of Down Syndrome, the segmental trisomy mouse (Ts65Dn). Ts65Dn mice survive to adulthood and have an extra chromosome that contains a segment of chromosome 16 homologous to human chromosome 21. In this study, field excitatory postsynaptic potentials (fEPSP) were recorded from the CA1 area of in vitro hippocampal slices from diploid and Ts65Dn mice, and LTP was induced by a single tetanizing pulse train (1 sec in duration) at 100 Hz. The hippocampus from both young (2 months) and older (9 months) Ts65Dn mice had a reduced LTP over a period of 60 min compared with LTP in age-matched controls. This finding may explain the reported behavioral and learning impairments in Ts65Dn mice; it suggests that this mouse model can be used to study the role of altered synaptic plasticity in mental retardation of Down Syndrome.
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