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

doi:10.1016/j.neulet.2011.06.043

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 journal › Article › peer-review

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 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.

Original language	English (US)
Pages (from-to)	212-215
Number of pages	4
Journal	Neuroscience Letters
Volume	500
Issue number	3
DOIs	https://doi.org/10.1016/j.neulet.2011.06.043
State	Published - Aug 18 2011

Funding

APP/PS1 mice were a generous gift from Dr. David Borchelt, John Hopkins University, Baltimore. Funding for this study was generously provided by the NIH ( MH077120 , AG026051 (MF); AG028072, RR00163 (HR)).

Funders	Funder number
Author National Institutes of Health National Institutes of Health National Institutes of Health National Institutes of Health The Bev Hartig Huntington's Disease Foundation National Institutes of Health	AG028072, RR00163, MH077120
National Institute of Aging	R03AG026051

Keywords

Alzheimer's
Amyloid
Glutamate
Hippocampus
Synaptic

ASJC Scopus subject areas

General Neuroscience

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10.1016/j.neulet.2011.06.043

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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 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.",

keywords = "Alzheimer's, Amyloid, Glutamate, Hippocampus, Synaptic",

author = "Ricoy, \{Ulises M.\} and Peizhong Mao and Maria Manczak and Reddy, \{P. Hemachandra\} and Frerking, \{Matthew E.\}",

note = "Funding Information: APP/PS1 mice were a generous gift from Dr. David Borchelt, John Hopkins University, Baltimore. Funding for this study was generously provided by the NIH ( MH077120 , AG026051 (MF); AG028072, RR00163 (HR)).",

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doi = "10.1016/j.neulet.2011.06.043",

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AU - Mao, Peizhong

AU - Manczak, Maria

AU - Reddy, P. Hemachandra

AU - Frerking, Matthew E.

N1 - Funding Information: APP/PS1 mice were a generous gift from Dr. David Borchelt, John Hopkins University, Baltimore. Funding for this study was generously provided by the NIH ( MH077120 , AG026051 (MF); AG028072, RR00163 (HR)).

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Y1 - 2011/8/18

N2 - 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.

AB - 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.

KW - Alzheimer's

KW - Amyloid

KW - Glutamate

KW - Hippocampus

KW - Synaptic

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

Abstract

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Keywords

ASJC Scopus subject areas

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