A transgenic mouse model for Alzheimer's disease has impaired synaptic gain but normal synaptic dynamics

Ulises M. Ricoy, Peizhong Mao, Maria Manczak, P. Hemachandra Reddy, Matthew E. Frerking

Research output: Contribution to journalArticle

5 Scopus citations

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 APPSwe/PS-1A246E 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 APPSwe/PS-1A246E 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.

Original languageEnglish (US)
Pages (from-to)212-215
Number of pages4
JournalNeuroscience Letters
Volume500
Issue number3
DOIs
StatePublished - Aug 18 2011

Keywords

  • Alzheimer's
  • Amyloid
  • Glutamate
  • Hippocampus
  • Synaptic

ASJC Scopus subject areas

  • Neuroscience(all)

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