Acute intracerebral treatment with amyloid-beta (1â€“42) alters the profile of neuronal oscillations that accompany LTP induction and results in impaired LTP in freely behaving rats

Kalweit, Alexander Nikolai; Yang, Honghong; Colitti-Klausnitzer, Jens; Fülöp, Lívia; Bozsó, Zsolt; Penke, Botond; Manahan‐Vaughan, Denise

doi:10.3389/fnbeh.2015.00103

Cited by 30 publications

(40 citation statements)

References 101 publications

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“…Reduction in theta oscillation power has also been observed in other genetically modified AD mice models such as 3xTg (Mondragon-Rodriguez et al, 2018), CRND8 (Goutagny et al, 2013), and APP23 transgenic AD mice models (Ittner et al, 2014). However, in addition to the reduction of theta oscillation power, hypersynchrony and epileptic activities were also observed in transgenic AD mice models (Bezzina et al, 2015; Ittner et al, 2014; Palop and Mucke, 2010) which was absent in the AβO-injected mice in ours and other studies (Kalweit et al, 2015). Hence, long-term effects of AβO may cause differing effects on the hippocampal neural circuits, which will require further investigation.…”

Section: Discussionsupporting

confidence: 54%

“…In our study, we injected AβO into the hippocampus to create AβO pathology in vivo , a method adopted in many studies investigating the impact of AβO physiological and cognitive functions (Balducci et al, 2010; Brouillette et al, 2012; Cetin and Dincer, 2007; Faucher et al, 2015; Kalweit et al, 2015; Kim et al, 2014b; Nicole et al, 2016; Orban et al, 2010; Villette et al, 2010; Yi et al, 2018). After three weeks of recovery following AβO injection in SST-Cre and PV-Cre mice, we observed a significant reduction in peak power of theta oscillations across all hippocampal sublayers compared to that in control SST-Cre and PV-Cre mice (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…AβOs have deleterious effects on neurons and synapses, causing synaptic dysfunction (Lacor et al, 2004; Shankar et al, 2008) and neural death (Alberdi et al, 2010; De Felice et al, 2007; Decker et al, 2010). Experimentally, AβO have been injected into the hippocampus in vivo to investigate the effect of AβO in hippocampal network oscillations, synaptic plasticity, and behavioral memory performance (Kalweit et al, 2015; Kim et al, 2014b; Nicole et al, 2016; Orban et al, 2010; Villette et al, 2010; Yi et al, 2018). In these studies, hippocampal theta oscillation, which is important in providing a clock mechanism for spike phase coding in spatial information processing (Dragoi and Buzsaki, 2006; Lisman and Jensen, 2013; O’Keefe and Recce, 1993) and support synaptic plasticity (Bikbaev and Manahan-Vaughan, 2008; Buzsaki, 2002; Huerta and Lisman, 1993; Nyhus and Curran, 2012; Tsanov and Manahan-Vaughan, 2009), was impaired in AD by showing decreased power compared to normal conditions.…”

Section: Introductionmentioning

confidence: 99%

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Optogenetic activation of SST-positive interneurons restores hippocampal theta oscillation impairment induced by soluble amyloid beta oligomersin vivo

Chung¹,

Park²,

Jang³

et al. 2018

Preprint

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Abnormal accumulation of amyloid β oligomers (AβO) is a hallmark of Alzheimer's disease (AD), which leads to learning and memory deficits. Hippocampal theta oscillations that are critical in spatial navigation, learning and memory are impaired in AD. Since GABAergic interneurons, such as somatostatin-positive (SST+) and parvalbumin-positive (PV+)interneurons, are believed to play key roles in the hippocampal oscillogenesis, we asked whether AβO selectively impairs these SST+ and PV+ interneurons. To selectively manipulate SST+ or PV+ interneuron activity in mice with AβO pathology in vivo, we coinjected AβO and adeno-associated virus (AAV) for expressing floxed channelrhodopsin-2 (ChR2) into the hippocampus of SST-Cre or PV-Cre mice. Local field potential (LFP) recordings in vivo in these AβO-injected mice showed a reduction in the peak power of theta oscillations and desynchronization of spikes from CA1 pyramidal neurons relative to theta oscillations compared to those in control mice. Optogenetic-activation of SST+ but not PV+ interneurons in AβO-injected mice fully restored the peak power of theta oscillations and resynchronized the theta spike phases to a level observed in control mice. In vitro whole-cell voltage-clamp recordings in CA1 pyramidal neurons in hippocampal slices treated with AβO revealed that short-term plasticity of SST+ interneuron inhibitory inputs to CA1 pyramidal neurons at theta frequency were selectively disrupted while that of PV+ interneuron inputs were unaffected. Together, our results suggest that dysfunction in inputs from SST+ interneurons to CA1 pyramidal neurons may underlie the impairment of theta oscillations observed in AβO-injected mice in vivo. Our findings identify SST+ interneurons as a target for restoring theta-frequency oscillations in early AD.

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Optogenetic activation of SST-positive interneurons restores hippocampal theta oscillation impairment induced by soluble amyloid beta oligomersin vivo

Chung¹,

Park²,

Jang³

et al. 2018

Preprint

View full text Add to dashboard Cite

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“…The concentrations of the stock solutions were 1 mg/mL in distilled water; the aggregation time was 3h (25 °C, pH 3.5); the neutralization (to pH 7.5) was performed with NaOH (1 N). (Kalweit et al, 2015) The final concentrations of Aβ were 100 µg/mL. The standard medium content (mg/L) were: Ca 2+ 31.05; Mg 2+ 17.6; Na + 0.9; K + 0.25; Fe 2+ 0.001; HCO3 -153.097; SO4 -3; Cl -0.8; F -0.02; H2SiO3 3.3 (pH=7.5).…”

Section: Methodsmentioning

confidence: 99%

Neurodegeneration-related beta-amyloid as autocatabolism-attenuator in amicro-in vivosystem

Balázs

Gálik-Oláh

Gálik

et al. 2020

Preprint

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StatementIn our current work we investigated the neurodegeneration-related and well-known neurotoxic beta-amyloid aggregate as an attenuator of autocatabolism-based organ shrinkage in an invertebrate micro-in vivo system. AbstractInvestigation of human neurodegeneration-related aggregates of beta-amyloid 1-42 (Aβ42) on bdelloid rotifers is a novel interdisciplinary approach in life sciences. We reapplied an organ size-based in vivo monitoring system, exploring the autocatabolism-related alterations evoked by Aβ42, in a glucosesupplemented starvation model. The experientially easy-to-follow size reduction of the bilateral reproductive organ (germovitellaria) in fasted rotifers was rescued by Aβ42, serving as a nutrient sourceand peptide sequence-specific attenuator of the organ shrinkage phase and enhancer of the regenerative one including egg reproduction. Recovery of the germovitellaria was significant in comparison with the greatly shrunken form. In contrast to the well-known neurotoxic Aβ42 (except the bdelloids) with specific regulatory roles, the artificially designed scrambled version (random order of amino acids) was inefficient in autocatabolism attenuation, behaving as negative control. This native Aβ42-related modulation of the 'functionally reversible organ shrinkage' can be a potential experiential and supramolecular marker of autocatabolism in vivo.

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“…The Aβ solutions with different aggregation state were prepared according to literature protocols. [36,39] …”

Section: Detection Of Aβ Oligomers By Elisamentioning

confidence: 99%

Multivalent foldamer-based affinity assay for selective recognition of Aβ oligomers

Olajos

Bartus

Schuster

et al. 2017

Analytica Chimica Acta

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Mimicking the molecular recognition functionality of antibodies is a great challenge. Foldamers are attractive candidates because of their relatively small size and designable interaction surface. This paper describes a sandwich type enzyme-linked immunoassay with a tetravalent β-peptide foldamer helix array as capture element and enzyme labeled tracer antibodies. The assay was found to be selective to β-amyloid oligomeric species with surface features transiently present in ongoing aggregation. In optimized conditions, with special emphasis on the foldamer immobilization, a detection limit of 5 pM was achieved with a linear range of 10 -500 pM. These results suggest that protein mimetic foldamers can be useful tools in biosensors and affinity assays.

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Acute intracerebral treatment with amyloid-beta (1â€“42) alters the profile of neuronal oscillations that accompany LTP induction and results in impaired LTP in freely behaving rats

Cited by 30 publications

References 101 publications

Optogenetic activation of SST-positive interneurons restores hippocampal theta oscillation impairment induced by soluble amyloid beta oligomersin vivo

Optogenetic activation of SST-positive interneurons restores hippocampal theta oscillation impairment induced by soluble amyloid beta oligomersin vivo

Neurodegeneration-related beta-amyloid as autocatabolism-attenuator in amicro-in vivosystem

Multivalent foldamer-based affinity assay for selective recognition of Aβ oligomers

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