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Activation of nicotinic α(7) acetylcholine receptor enhances long term potentation in wild type mice but not in APP(swe)/PS1ΔE9 mice

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@article{6bc285e69bd6475bb5649c672f7fc8c3,
title = "Activation of nicotinic α(7) acetylcholine receptor enhances long term potentation in wild type mice but not in APP(swe)/PS1ΔE9 mice",
abstract = "Amyloid β (Aβ) plays a central role in Alzheimer's disease (AD) and binds to the nicotinic α(7) receptor (α(7) nAChR). Little is known about the degree to which the binding of Aβ to the α(7) nAChR influences the role of this receptor in long-term potentiation (LTP), however. We have studied the effect of the partial α(7) nAChR agonist SSR180711 on hippocampal slice preparations from normal wild type (Wt) and APP(swe)/PS1ΔE9 transgenic (Tg) mice. In the hippocampal slices from the 6 months old Wt mice, the application of both nicotine (5μM) and SSR180711 (300nM) resulted in a significant enhancement of LTP expressed in area CA1. However, in the Tg mice the application of SSR180711 did not result in an increase in LTP beyond control levels. The amount of binding of the α(7) nAChR ligand 125-I-α-bungarotoxin was not different between in Tg and Wt mice. These findings indicate that the α(7) nAChR is functionally blocked in the hippocampal neurons, downstream of the α(7) nAChR, and that this is likely due to an interaction between the receptor and Aβ, which leads to changes in LTP.",
keywords = "Amyloid beta-Protein Precursor, Animals, Bicyclo Compounds, Heterocyclic, Excitatory Postsynaptic Potentials, Female, Hippocampus, Humans, Long-Term Potentiation, Mice, Mice, Transgenic, Nicotine, Nicotinic Agonists, Organ Culture Techniques, RNA-Binding Proteins, Receptors, Nicotinic, Ribosomal Proteins",
author = "Andreas S{\"o}derman and Mikkelsen, {Jens D} and West, {Mark J.} and Christensen, {Ditte Z} and Jensen, {Morten S}",
note = "Copyright {\^A}{\textcopyright} 2010 Elsevier Ireland Ltd. All rights reserved.",
year = "2011",
doi = "10.1016/j.neulet.2010.10.049",
language = "English",
volume = "487",
pages = "325--9",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "3",

}

RIS

TY - JOUR

T1 - Activation of nicotinic α(7) acetylcholine receptor enhances long term potentation in wild type mice but not in APP(swe)/PS1ΔE9 mice

AU - Söderman, Andreas

AU - Mikkelsen, Jens D

AU - West, Mark J.

AU - Christensen, Ditte Z

AU - Jensen, Morten S

N1 - Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.

PY - 2011

Y1 - 2011

N2 - Amyloid β (Aβ) plays a central role in Alzheimer's disease (AD) and binds to the nicotinic α(7) receptor (α(7) nAChR). Little is known about the degree to which the binding of Aβ to the α(7) nAChR influences the role of this receptor in long-term potentiation (LTP), however. We have studied the effect of the partial α(7) nAChR agonist SSR180711 on hippocampal slice preparations from normal wild type (Wt) and APP(swe)/PS1ΔE9 transgenic (Tg) mice. In the hippocampal slices from the 6 months old Wt mice, the application of both nicotine (5μM) and SSR180711 (300nM) resulted in a significant enhancement of LTP expressed in area CA1. However, in the Tg mice the application of SSR180711 did not result in an increase in LTP beyond control levels. The amount of binding of the α(7) nAChR ligand 125-I-α-bungarotoxin was not different between in Tg and Wt mice. These findings indicate that the α(7) nAChR is functionally blocked in the hippocampal neurons, downstream of the α(7) nAChR, and that this is likely due to an interaction between the receptor and Aβ, which leads to changes in LTP.

AB - Amyloid β (Aβ) plays a central role in Alzheimer's disease (AD) and binds to the nicotinic α(7) receptor (α(7) nAChR). Little is known about the degree to which the binding of Aβ to the α(7) nAChR influences the role of this receptor in long-term potentiation (LTP), however. We have studied the effect of the partial α(7) nAChR agonist SSR180711 on hippocampal slice preparations from normal wild type (Wt) and APP(swe)/PS1ΔE9 transgenic (Tg) mice. In the hippocampal slices from the 6 months old Wt mice, the application of both nicotine (5μM) and SSR180711 (300nM) resulted in a significant enhancement of LTP expressed in area CA1. However, in the Tg mice the application of SSR180711 did not result in an increase in LTP beyond control levels. The amount of binding of the α(7) nAChR ligand 125-I-α-bungarotoxin was not different between in Tg and Wt mice. These findings indicate that the α(7) nAChR is functionally blocked in the hippocampal neurons, downstream of the α(7) nAChR, and that this is likely due to an interaction between the receptor and Aβ, which leads to changes in LTP.

KW - Amyloid beta-Protein Precursor

KW - Animals

KW - Bicyclo Compounds, Heterocyclic

KW - Excitatory Postsynaptic Potentials

KW - Female

KW - Hippocampus

KW - Humans

KW - Long-Term Potentiation

KW - Mice

KW - Mice, Transgenic

KW - Nicotine

KW - Nicotinic Agonists

KW - Organ Culture Techniques

KW - RNA-Binding Proteins

KW - Receptors, Nicotinic

KW - Ribosomal Proteins

U2 - 10.1016/j.neulet.2010.10.049

DO - 10.1016/j.neulet.2010.10.049

M3 - Journal article

C2 - 20974225

VL - 487

SP - 325

EP - 329

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 3

ER -

ID: 33247814