ArticleBritish journal of pharmacology2012
A β-amyloid oligomer directly modulates P/Q-type calcium currents in Xenopus oocytes.
Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Role of Ion Channels in Alzheimer's Disease Pathophysiology.The Journal of membrane biology · 2025Review
- Article
- Distinct Disruptions in CA1 and CA3 Place Cell Function in Alzheimer's Disease Mice.bioRxiv : the preprint server for biology · 2024Article
- Review
- Protofibrillar Amyloid Beta Modulation of Recombinant hCaV2.2 (N-Type) Voltage-Gated Channels.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Hippocampal Degeneration and Behavioral Impairment During Alzheimer-Like Pathogenesis Involves Glutamate Excitotoxicity.Journal of molecular neuroscience : MN · 2021Article
- Out-of-Register Parallel β-Sheets and Antiparallel β-Sheets Coexist in 150-kDa Oligomers Formed by Amyloid-β(1-42).Journal of molecular biology · 2020Article
- Amyloid β oligomers suppress excitatory transmitter release via presynaptic depletion of phosphatidylinositol-4,5-bisphosphate.Nature communications · 2019Article
- The Acute Effects of Amyloid-BetaFrontiers in neuroscience · 2019Article
- SUMOylation and calcium signalling: potential roles in the brain and beyond.Neuronal signaling · 2017Review
- Inhibiting BACE1 to reverse synaptic dysfunctions in Alzheimer's disease.Neuroscience and biobehavioral reviews · 2016Review
- Neuronal Network Oscillations in Neurodegenerative Diseases.Neuromolecular medicine · 2015Review
- Posttraumatic stress disorder-like induction elevates β-amyloid levels, which directly activates corticotropin-releasing factor neurons to exacerbate stress responses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Calcium channel blockers and dementia.British journal of pharmacology · 2013Review
- Treadmill exercise prevents learning and memory impairment in Alzheimer's disease-like pathology.Current Alzheimer research · 2013Article
- The changing landscape of voltage-gated calcium channels in neurovascular disorders and in neurodegenerative diseases.Current neuropharmacology · 2013Article
- Ablation of Ca(V)2.1 voltage-gated Ca²⁺ channels in mouse forebrain generates multiple cognitive impairments.PloS one · 2013Article
- P/Q-type calcium channel modulators.British journal of pharmacology · 2012Review
- Functional and structural effects of amyloid-β aggregate on Xenopus laevis oocytes.Molecules and cells · 2012Article
- Alzheimer's disease, β-amyloid, glutamate, NMDA receptors and memantine--searching for the connections.British journal of pharmacology · 2012Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeβ-amyloid (Aβ) oligomers have been implicated in the early pathophysiology of Alzheimer's disease (AD). While the precise nature of the molecular target has not been fully revealed, a number of studies have indicated that Aβ oligomers modulate neuron-specific ion channels. We recently provided evidence that Aβ oligomers suppress isolated P/Q-type calcium currents in cultured nerve cells. Using a heterologous expression system, we aimed to prove a direct effect on the membrane channel mediating such current. EXPERIMENTAL APPROACH: The effects of a synthetically generated Aβ oligomer, Aβ globulomer, were investigated on P/Q-type currents recorded from Xenopus laevis oocytes expressing the full P/Q-type calcium channel or the pore-forming subunit only. We also examined the effects of Aβ globulomer on recombinant NMDA receptor currents. Finally, we compared the modulation by Aβ globulomer with that induced by a synthetic monomeric Aβ. KEY
resultsAβ globulomer directly and dose-dependently modulated P/Q-type calcium channels. A leftward shift of the current-voltage curve indicated that the threshold for channel opening was reduced. The effect of Aβ globulomer was also present when only the α1A subunit of the normally tripartite channel was expressed. In contrast, the monomeric Aβ had no effect on P/Q current. Also globulomer Aβ had no effect on glutamate-induced NMDA currents. CONCLUSIONS AND IMPLICATIONS: The α1A subunit of the P/Q-type calcium channel is directly modulated by oligomeric Aβ. Threshold reduction as well as an increase in current at synaptic terminals may facilitate vesicle release and could trigger excitotoxic events in the brains of patients with AD.
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