Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo

Nature ◽  
2002 ◽  
Vol 416 (6880) ◽  
pp. 535-539 ◽  
Author(s):  
Dominic M. Walsh ◽  
Igor Klyubin ◽  
Julia V. Fadeeva ◽  
William K. Cullen ◽  
Roger Anwyl ◽  
...  
Keyword(s):  
Amyloid Β ◽  
Long Term Potentiation ◽  
Amyloid Β Protein ◽  
Β Protein ◽  
Term Potentiation

[Gly14]-humanin rescues long-term potentiation from amyloid β protein-induced impairment in the rat hippocampal CA1 region in vivo

Synapse ◽  
2010 ◽  
Vol 64 (1) ◽  
pp. 83-91 ◽  
Author(s):  
Fen Guo ◽  
Wei Jing ◽  
Cun-Gen Ma ◽  
Mei-Na Wu ◽  
Jun-Fang Zhang ◽  
...  
Keyword(s):  
Amyloid Β ◽  
Long Term Potentiation ◽  
Amyloid Β Protein ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Β Protein ◽  
Term Potentiation ◽  
Hippocampal Ca1

Amyloid-β oligomers: their production, toxicity and therapeutic inhibition

2002 ◽  
Vol 30 (4) ◽  
pp. 552-557 ◽  
Author(s):  
D. M. Walsh ◽  
I. Klyubin ◽  
J. V. Fadeeva ◽  
M. J. Rowan ◽  
D. J. Selkoe
Keyword(s):  
Amyloid Β ◽  
Long Term Potentiation ◽  
Specific Form ◽  
Amyloid Β Protein ◽  
Β Protein ◽  
Term Potentiation ◽  
Modelling Data

Despite extensive genetic and animal modelling data that support a central role for the amyloid β-protein (Aβ) in the genesis of Alzheimer's disease, the specific form(s) of Aβ which causes injury to neurons in vivo has not been identified. In the present study, we examine the importance of soluble, pre-fibrillar assemblies of Aβ as mediators of neurotoxicity. Specifically, we review the role of cell-derived SDS-stable oligomers, their blocking of hippocampal long-term potentiation in vivo and the finding that this blocking can be prevented by prior treatment of oligomer-producing cells withγ-secretase inhibitors.

Amyloid β-protein fragment 31–35 suppresses long-term potentiation in hippocampal CA1 region of rats in vivo

Synapse ◽  
2006 ◽  
Vol 60 (4) ◽  
pp. 307-313 ◽  
Author(s):  
Jian-Mei Zhang ◽  
Mei-Na Wu ◽  
Jin-Shun Qi ◽  
Jian-Tian Qiao
Keyword(s):  
Amyloid Β ◽  
Long Term Potentiation ◽  
Amyloid Β Protein ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Β Protein ◽  
Term Potentiation ◽  
Hippocampal Ca1

Arginine vasopressin prevents amyloid β protein-induced impairment of long-term potentiation in rat hippocampus in vivo

2009 ◽  
Vol 450 (3) ◽  
pp. 306-310 ◽  
Author(s):  
Wei Jing ◽  
Fen Guo ◽  
Li Cheng ◽  
Jun-Fang Zhang ◽  
Jin-Shun Qi
Keyword(s):  
Arginine Vasopressin ◽  
Amyloid Β ◽  
Long Term Potentiation ◽  
Rat Hippocampus ◽  
Amyloid Β Protein ◽  
Β Protein ◽  
Term Potentiation

scholarly journals Transglutaminase Induces Protofibril-like Amyloid β-Protein Assemblies That Are Protease-resistant and Inhibit Long-term Potentiation

2008 ◽  
Vol 283 (24) ◽  
pp. 16790-16800 ◽  
Author(s):  
Dean M. Hartley ◽  
Chaohui Zhao ◽  
Austin C. Speier ◽  
Gavitt A. Woodard ◽  
Shaomin Li ◽  
...  
Keyword(s):  
Amyloid Β ◽  
Long Term Potentiation ◽  
Amyloid Β Protein ◽  
Protein Assemblies ◽  
Β Protein ◽  
Term Potentiation

scholarly journals Role of GirK Channels in Long-Term Potentiation of Synaptic Inhibition in an In Vivo Mouse Model of Early Amyloid-β Pathology

2019 ◽  
Vol 20 (5) ◽  
pp. 1168 ◽  
Author(s):  
Irene Sánchez-Rodríguez ◽  
Agnès Gruart ◽  
José Delgado-García ◽  
Lydia Jiménez-Díaz ◽  
Juan Navarro-López
Keyword(s):  
Mouse Model ◽  
Amyloid Β ◽  
Long Term Potentiation ◽  
Synaptic Inhibition ◽  
Girk Channels ◽  
Girk Channel ◽  
Term Potentiation ◽  
Inhibitory Signaling

Imbalances of excitatory/inhibitory synaptic transmission occur early in the pathogenesis of Alzheimer’s disease (AD), leading to hippocampal hyperexcitability and causing synaptic, network, and cognitive dysfunctions. G-protein-gated potassium (GirK) channels play a key role in the control of neuronal excitability, contributing to inhibitory signaling. Here, we evaluate the relationship between GirK channel activity and inhibitory hippocampal functionality in vivo. In a non-transgenic mouse model of AD, field postsynaptic potentials (fPSPs) from the CA3–CA1 synapse in the dorsal hippocampus were recorded in freely moving mice. Intracerebroventricular (ICV) injections of amyloid-β (Aβ) or GirK channel modulators impaired ionotropic (GABAA-mediated fPSPs) and metabotropic (GirK-mediated fPSPs) inhibitory signaling and disrupted the potentiation of synaptic inhibition. However, the activation of GirK channels prevented Aβ-induced changes in GABAA components. Our data shows, for the first time, the presence of long-term potentiation (LTP) for both the GABAA and GirK-mediated inhibitory postsynaptic responses in vivo. In addition, our results support the importance of an accurate level of GirK-dependent signaling for dorsal hippocampal performance in early amyloid pathology models by controlling the excess of excitation that disrupts synaptic plasticity processes.

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