Restoring long-term potentiation impaired by amyloid-beta oligomers: Comparison of an acetylcholinesterase inhibitior and selective neuronal nicotinic receptor agonists

Kroker, Katja S.; Moreth, Jens; Kußmaul, Lothar; Rast, Georg; Rosenbrock, Holger

doi:10.1016/j.brainresbull.2013.04.006

Cited by 23 publications

(20 citation statements)

References 131 publications

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“…Note that other studies have reported that working at similar temperatures does not impair the ability of Aβ1–42 to reduce LTP (Kroker et al, 2013; Nomura et al, 2005; Nomura et al, 2012; Rammes et al, 2011). Slices were prepared by standard methods (Madison and Nicoll, 1986).…”

Section: Methodsmentioning

confidence: 76%

“…It remains the most compelling model for a learning mechanism at the synaptic level (Bliss and Collingridge, 1993). In general, application of sub-micro molar concentrations of Aβ to hippocampal tissue has been reported to result in a reduction in LTP (Chen et al, 2000; Cullen et al, 1997; Freir et al, 2001; Gengler et al, 2007; Kim et al, 2013; Klyubin et al, 2004; Kroker et al, 2013; Lambert et al, 1998; Nomura et al, 2005; Nomura et al, 2012; Rammes et al, 2011; Raymond et al, 2003; Ronicke et al, 2008; Rowan et al, 2004; Townsend et al, 2006b; Vitolo et al, 2002; Walsh et al, 2002; Wang et al, 2002a; Wang et al, 2004b) leading to speculation that this is a critical path by which Aβ may impair learning and/or memory.…”

Section: Introductionmentioning

confidence: 99%

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β-Amyloid Inhibits E-S Potentiation through Suppression of Cannabinoid Receptor 1-Dependent Synaptic Disinhibition

Orr

Hanson

Liu

et al. 2014

Neuron

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Summary It has been widely reported that β-amyloid peptide (Aβ) blocks long-term potentiation (LTP) of hippocampal synapses. Here we show evidence that Aβ more potently blocks the potentiation of excitatory post-synaptic potential (EPSP) -spike coupling (E-S potentiation). This occurs not by direct effect on excitatory synapses or postsynaptic neurons, but rather through a novel indirect mechanism: reduction of endocannabinoid-mediated peri-tetanic disinhibition. During high frequency (tetanic) stimulation, somatic synaptic inhibition is suppressed by endocannabinoids. We find that Aβ prevents this endocannabinoid-mediated disinhibition, thus leaving synaptic inhibition more intact during tetanic stimulation. This intact inhibition opposes the normal depolarization of hippocampal pyramidal neurons that occurs during tetanus, thus opposing the induction of synaptic plasticity. Thus, a novel pathway through which Aβ can act to modulate neural activity is identified, relevant to learning and memory and how it may mediate aspects of the cognitive decline seen in Alzheimer's disease.

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Section: Methodsmentioning

confidence: 76%

Section: Introductionmentioning

confidence: 99%

β-Amyloid Inhibits E-S Potentiation through Suppression of Cannabinoid Receptor 1-Dependent Synaptic Disinhibition

Orr

Hanson

Liu

et al. 2014

Neuron

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“…The last difference seems to be the most important. Kroker et al (2012Kroker et al ( , 2013 recorded fEPSPs and did not find a pronounced effect of donepezil on A␤-impaired LTP. We recorded PSs and did find the reversal of A␤-impaired LTP by donepezil and PRE-084.…”

Section: Discussionmentioning

confidence: 85%

“…Given multiple membrane and cytoplasmic molecular targets sensitive to A␤, it is not surprising that many different approaches can ameliorate cytotoxic action of A␤ including LTP deficits. The reversal of LTP impaired by A␤ was observed with administration of a number of substances, namely antioxidant SkQ1 (Kapay et al, 2013), calcineurin inhibitors FK506 and cyclosporine (Chen et al, 2002), ␣7nAChR partial agonist SSR180711 (Kroker et al, 2013), mGluR5 antagonist MPEP (Rammes et al, 2011;Wang et al, 2004), inhibitor of AChE (-)huperzine A (Ye and Qiao, 1999). Our work has extended this list by adding substances such as agonists of Sig1-R donepezil and PRE-084.…”

Section: Discussionmentioning

confidence: 90%

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The involvement of sigma1 receptors in donepezil-induced rescue of hippocampal LTP impaired by beta-amyloid peptide

Solntseva

Kapai

Попова

et al. 2014

Brain Research Bulletin

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Age‐related synaptic dysfunction in Tg2576 mice starts as a failure in early long‐term potentiation which develops into a full abolishment of late long‐term potentiation

Fernández-Fernández

Dorner-Ciossek

Kroker

et al. 2015

J of Neuroscience Research

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Tg2576 mice are widely used to study amyloid-dependent synaptic dysfunction related to Alzheimer's disease. However, conflicting data have been reported for these mice with regard to basal transmission as well as the in vitro correlate of memory, long-term potentiation (LTP). Some studies show clear impairments, whereas others report no deficiency. The present study uses hippocampal slices from 3-, 10-, and 15-month-old wild-type (WT) and Tg2576 mice to evaluate synaptic function in each group, including experiments to investigate basal synaptic transmission, short- and long-term plasticity by inducing paired-pulse facilitation, and both early and late LTP. We show that synaptic function remains intact in hippocampal slices from Tg2576 mice at 3 months of age. However, both early and late LTP decline progressively during aging in these mice. This deterioration of synaptic plasticity starts affecting early LTP, ultimately leading to the abolishment of both forms of LTP in 15-month-old animals. In comparison, WT littermates display normal synaptic parameters during aging. Additional pharmacological investigation into the involvement of NMDA receptors and L-type voltage-gated calcium channels in LTP suggests a distinct mechanism of induction among age groups, demonstrating that both early and late LTP are differentially affected by these channels in Tg2576 mice during aging.

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Restoring long-term potentiation impaired by amyloid-beta oligomers: Comparison of an acetylcholinesterase inhibitior and selective neuronal nicotinic receptor agonists

Cited by 23 publications

References 131 publications

β-Amyloid Inhibits E-S Potentiation through Suppression of Cannabinoid Receptor 1-Dependent Synaptic Disinhibition

β-Amyloid Inhibits E-S Potentiation through Suppression of Cannabinoid Receptor 1-Dependent Synaptic Disinhibition

The involvement of sigma1 receptors in donepezil-induced rescue of hippocampal LTP impaired by beta-amyloid peptide

Age‐related synaptic dysfunction in Tg2576 mice starts as a failure in early long‐term potentiation which develops into a full abolishment of late long‐term potentiation

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