Synaptic Fatigue is More Pronounced in the APP/PS1 Transgenic Mouse Model of Alzheimers Disease

Author(s): Hong Zhang, Bing Gong, Shumin Liu, Mauro Fa, Ipe Ninan, Agnieszka Staniszewski, Ottavio Arancio

Journal Name: Current Alzheimer Research

Volume 2 , Issue 2 , 2005

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To search for potential mechanism that might alter synaptic transmission following Aβ increase we have examined the presynaptic component of transmitter release. As parameters of synaptic transmission that might underlie presynaptic mechanisms, we have used paired-pulse facilitation (PPF), post-tetanic potentiation (PTP), and synaptic fatigue (SF) at the connection between the hippocampal Schaffer-collateral pathway and CA1 pyramidal neurons in ∼5 month old double transgenic mice overexpressing the mutated form of amyloid precursor protein (APPK670N, M671L) and presenilin 1 (PS1M146V). While the presynaptic mechanisms of PPF and PTP were not compromised in the APP / PS1 mice, SF was more pronounced in the double transgenic animals. The percentage of the 40th fEPSP slope over the first during the tetanus was 18 ± 3% in APP / PS1 vs. 26 ± 2% in WT. Thus, it is likely that presynaptic mechanisms underlying SF but not PPF and PTP, may account for synaptic dysfunction in APP / PS1 mice.

Keywords: synapse, amyloid, synaptic fatigue, post-tetanic potentiation, paired pulse facilitation, neurotransmitter release, alzheimers disease

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Article Details

Year: 2005
Published on: 01 March, 2012
Page: [137 - 140]
Pages: 4
DOI: 10.2174/1567205053585936
Price: $65

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