title: A transgenic mouse model for Alzheimer's disease has impaired synaptic gain but normal synaptic dynamics.
abstract: The chronic accumulation of amyloid beta (Aβ) peptides is thought to underlie much of the pathology of Alzheimer's disease (AD), and transgenic mice overexpressing Aβ 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 Aβ impairs synaptic transmission through a reduction in the synaptic gain, while preserving the synaptic dynamics.
authors: Department of Behavioral Neuroscience, Oregon Health and Science University, 3181 SW Sam Jackson Pk Rd., Portland, OR 97239, United States.
authors: Ulises M
authors: UM
authors: Ricoy
authors: Peizhong
authors: P
authors: Mao
authors: Maria
authors: M
authors: Manczak
authors: P Hemachandra
authors: PH
authors: Reddy
authors: Matthew E
authors: ME
authors: Frerking
mesh_terms: D000544:Alzheimer Disease / Q000235:genetics / Q000503:physiopathology*; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D000818:Animals; D019706:Excitatory Postsynaptic Potentials; D006624:Hippocampus / Q000503:physiopathology; D066298:In Vitro Techniques; D051379:Mice; D008822:Mice, Transgenic; D053764:Presenilin-1 / Q000235:genetics; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission
chemical_list: D016564:Amyloid beta-Protein Precursor; D053764:Presenilin-1