scholarly journals Differential Inhibition of E-S Potentiation and Long-term Potentiation by Cell-Derived and Arctic Amyloid Beta

2020 ◽  
Vol 4 (1) ◽  
Author(s):  
Adrienne L Orr ◽  
Jason K Clark ◽  
Daniel V Madison
Keyword(s):  
Amyloid Beta ◽  
Long Term Potentiation ◽  
Differential Inhibition ◽  
Term Potentiation

scholarly journals Differential Inhibition of E-S Potentiation and Long-term Potentiation by Cell-derived and Arctic Amyloid Beta

2019 ◽  
Author(s):  
Adrienne L. Orr ◽  
Jason K. Clark ◽  
Daniel V. Madison
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Hippocampal Slices ◽  
Memory Deficits ◽  
Long Term Potentiation ◽  
Amyloid Beta Peptide ◽  
Term Potentiation ◽  
Beta Peptide

AbstractSoluble oligomers of amyloid-beta peptide (Abeta) have been implicated in the onset of memory deficits in Alzheimer’s disease, perhaps due to their reported ability to impair long-term potentiation (LTP) of synaptic strength. We previously showed the effect of Abeta on LTP depends on the strength of LTP induction. Furthermore, Abeta affects EPSP-Spike (E-S) potentiation more robustly than LTP, suggesting that E-S potentiation may be equally important to learning and memory in the context of Alzheimer’s disease. Here we extend our findings to two additional forms of Abeta that form higher concentrations of soluble Abeta oligomers and show that they also affect E-S potentiation at induction strengths where there is no effect on LTP in hippocampal slices.

Short erythropoietin-derived peptide enhances memory, improves long-term potentiation, and counteracts amyloid beta–induced pathology

2019 ◽  
Vol 81 ◽  
pp. 88-101 ◽  
Author(s):  
Oksana Dmytriyeva ◽  
Amor Belmeguenai ◽  
Laurent Bezin ◽  
Katia Soud ◽  
David Paul Drucker Woldbye ◽  
...  
Keyword(s):  
Amyloid Beta ◽  
Long Term Potentiation ◽  
Term Potentiation

Soluble Arctic amyloid beta protein inhibits hippocampal long-term potentiation in vivo

2004 ◽  
Vol 19 (10) ◽  
pp. 2839-2846 ◽  
Author(s):  
Igor Klyubin ◽  
Dominic M. Walsh ◽  
William K. Cullen ◽  
Julia V. Fadeeva ◽  
Roger Anwyl ◽  
...  
Keyword(s):  
Amyloid Beta ◽  
Long Term Potentiation ◽  
Amyloid Beta Protein ◽  
Term Potentiation

scholarly journals Pharmacological Modulation of Three Modalities of CA1 Hippocampal Long-Term Potentiation in the Ts65Dn Mouse Model of Down Syndrome

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Jonah J. Scott-McKean ◽  
Adriano L. Roque ◽  
Krystyna Surewicz ◽  
Mark W. Johnson ◽  
Witold K. Surewicz ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Amyloid Beta ◽  
Past Research ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Detectable Effect ◽  
Ts65dn Mouse ◽  
Term Potentiation ◽  
Frequency Stimulation

The Ts65Dn mouse is the most studied animal model of Down syndrome. Past research has shown a significant reduction in CA1 hippocampal long-term potentiation (LTP) induced by theta-burst stimulation (TBS), but not in LTP induced by high-frequency stimulation (HFS), in slices from Ts65Dn mice compared with euploid mouse-derived slices. Additionally, therapeutically relevant doses of the drug memantine were shown to rescue learning and memory deficits in Ts65Dn mice. Here, we observed that 1 μM memantine had no detectable effect on HFS-induced LTP in either Ts65Dn- or control-derived slices, but it rescued TBS-induced LTP in Ts65Dn-derived slices to control euploid levels. Then, we assessed LTP induced by four HFS (4xHFS) and found that this form of LTP was significantly depressed in Ts65Dn slices when compared with LTP in euploid control slices. Memantine, however, did not rescue this phenotype. Because 4xHFS-induced LTP had not yet been characterized in Ts65Dn mice, we also investigated the effects of picrotoxin, amyloid beta oligomers, and soluble recombinant human prion protein (rPrP) on this form of LTP. Whereas ≥10 μM picrotoxin increased LTP to control levels, it also caused seizure-like oscillations. Neither amyloid beta oligomers nor rPrP had any effect on 4xHFS-induced LTP in Ts65Dn-derived slices.

The NMDA receptor antagonist Radiprodil reverses the synaptotoxic effects of different amyloid-beta (Aβ) species on long-term potentiation (LTP)

2018 ◽  
Vol 140 ◽  
pp. 184-192 ◽  
Author(s):  
Gerhard Rammes ◽  
Franziska Seeser ◽  
Korinna Mattusch ◽  
Kaichuan Zhu ◽  
Laura Haas ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Amyloid Beta ◽  
Long Term Potentiation ◽  
Nmda Receptor Antagonist ◽  
Term Potentiation

P2-399: RESTORING LONG-TERM POTENTIATION IMPAIRED BY AMYLOID-BETA OLIGOMERS: COMPARISON OF A BROADLY-SPECIFIC ANTI AMYLOID-BETA NANOBODY AND A MONOMER-SPECIFIC ANTIBODY

2014 ◽  
Vol 10 ◽  
pp. P625-P625
Author(s):  
Katja Kroker ◽  
Scott Hobson ◽  
Holger Rosenbrock ◽  
Thorsten Lamla ◽  
Jo Vercammen ◽  
...  
Keyword(s):  
Amyloid Beta ◽  
Specific Antibody ◽  
Long Term Potentiation ◽  
Term Potentiation

scholarly journals Amyloid Beta-Related Alterations to Glutamate Signaling Dynamics During Alzheimer’s Disease Progression

ASN NEURO ◽  
2019 ◽  
Vol 11 ◽  
pp. 175909141985554 ◽  
Author(s):  
Caleigh A. Findley ◽  
Andrzej Bartke ◽  
Kevin N. Hascup ◽  
Erin R. Hascup
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Progression ◽  
Amyloid Beta ◽  
Cognitive Deficits ◽  
Senile Plaques ◽  
Neuronal Loss ◽  
Long Term Potentiation ◽  
Term Potentiation

Alzheimer’s disease (AD) ranks sixth on the Centers for Disease Control and Prevention Top 10 Leading Causes of Death list for 2016, and the Alzheimer’s Association attributes 60% to 80% of dementia cases as AD related. AD pathology hallmarks include accumulation of senile plaques and neurofibrillary tangles; however, evidence supports that soluble amyloid beta (Aβ), rather than insoluble plaques, may instigate synaptic failure. Soluble Aβ accumulation results in depression of long-term potentiation leading to cognitive deficits commonly characterized in AD. The mechanisms through which Aβ incites cognitive decline have been extensively explored, with a growing body of evidence pointing to modulation of the glutamatergic system. The period of glutamatergic hypoactivation observed alongside long-term potentiation depression and cognitive deficits in later disease stages may be the consequence of a preceding period of increased glutamatergic activity. This review will explore the Aβ-related changes to the tripartite glutamate synapse resulting in altered cell signaling throughout disease progression, ultimately culminating in oxidative stress, synaptic dysfunction, and neuronal loss.

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