| First Author | Ricoy UM | Year | 2011 |
| Journal | Neurosci Lett | Volume | 500 |
| Issue | 3 | Pages | 212-5 |
| PubMed ID | 21741442 | Mgi Jnum | J:174545 |
| Mgi Id | MGI:5139953 | Doi | 10.1016/j.neulet.2011.06.043 |
| Citation | Ricoy UM, et al. (2011) A transgenic mouse model for Alzheimer's disease has impaired synaptic gain but normal synaptic dynamics. Neurosci Lett 500(3):212-5 |
| abstractText | The chronic accumulation of amyloid beta (Abeta) peptides is thought to underlie much of the pathology of Alzheimer's disease (AD), and transgenic mice overexpressing Abeta show both behavioral defects and impairments in hippocampal synaptic transmission. In the present study, we examined excitatory transmission at the Schaffer collateral synapse in acute hippocampal slices from APP(Swe)/PS-1(A246E) transgenic mice to determine whether the synaptic impairment in these mice is due to a reduction in the activity-independent synaptic gain, or to a change in the activity-dependent synaptic dynamics. We observed a strong reduction in synaptic transmission in slices from APP(Swe)/PS-1(A246E) mice compared to those from their wildtype littermates. However, there was no resolvable change in the synaptic dynamics observed in response to either simple or complex stimulus trains. We conclude that the chronic accumulation of Abeta impairs synaptic transmission through a reduction in the synaptic gain, while preserving the synaptic dynamics. |
