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Publication : APP processing and synaptic plasticity in presenilin-1 conditional knockout mice.

First Author  Yu H Year  2001
Journal  Neuron Volume  31
Issue  5 Pages  713-26
PubMed ID  11567612 Mgi Jnum  J:71606
Mgi Id  MGI:2150480 Doi  10.1016/s0896-6273(01)00417-2
Citation  Yu H, et al. (2001) App processing and synaptic plasticity in presenilin-1 conditional knockout mice. Neuron 31(5):713-26
abstractText  We have developed a presenilin-1 (PS1) conditional knockout mouse (cKO), in which PS1 inactivation is restricted to the postnatal forebrain. The PS1 cKO mouse is viable and exhibits no gross abnormalities. The carboxy-terminal fragments of the amyloid precursor protein differentially accumulate in the cerebral cortex of cKO mice, while generation of beta-amyloid peptides is reduced. Expression of Notch downstream effector genes, Hes1, Hes5, and Dll1, is unaffected in the cKO cortex. Although basal synaptic transmission, long-term potentiation, and long-term depression at hippocampal area CA1 synapses are normal, the PS1 cKO mice exhibit subtle but significant deficits in long-term spatial memory. These results demonstrate that inactivation of PS1 function in the adult cerebral cortex leads to reduced Abeta generation and subtle cognitive deficits without affecting expression of Notch downstream genes.
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