ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Mossy fiber long-term potentiation deficits in BACE1 knock-outs can be rescued by activation of alpha7 nicotinic acetylcholine receptors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Neuronal and Glial α7 Nicotinic Acetylcholine Receptors: Role in Alzheimer's Disease Pathophysiology.Life (Basel, Switzerland) · 2025Review
- Physiological Roles of β-amyloid in Regulating Synaptic Function: Implications for AD Pathophysiology.Neuroscience bulletin · 2023Review
- BACE1 regulates expression of Clusterin in astrocytes for enhancing clearance of β-amyloid peptides.Molecular neurodegeneration · 2023Article
- BACE1 controls synaptic function through modulating release of synaptic vesicles.Molecular psychiatry · 2021Article
- Axonal organization defects in the hippocampus of adult conditional BACE1 knockout mice.Science translational medicine · 2018Article
- β-Secretase BACE1 Promotes Surface Expression and Function of Kv3.4 at Hippocampal Mossy Fiber Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Genetic Deletion of the Clathrin Adaptor GGA3 Reduces Anxiety and Alters GABAergic Transmission.PloS one · 2016Article
- The effect of α7 nicotinic receptor activation on glutamatergic transmission in the hippocampus.Biochemical pharmacology · 2015Review
- Extracellular proteolysis in structural and functional plasticity of mossy fiber synapses in hippocampus.Frontiers in cellular neuroscience · 2015Review
- Methylene blue modulates β-secretase, reverses cerebral amyloidosis, and improves cognition in transgenic mice.The Journal of biological chemistry · 2014Article
- Postsynaptic target specific synaptic dysfunctions in the CA3 area of BACE1 knockout mice.PloS one · 2014Article
- Possible contributions of a novel form of synaptic plasticity in Aplysia to reward, memory, and their dysfunctions in mammalian brain.Learning & memory (Cold Spring Harbor, N.Y.) · 2013Review
- Opposing actions of environmental enrichment and Alzheimer's disease on the expression of hippocampal microRNAs in mouse models.Translational psychiatry · 2013Article
- M2 muscarinic acetylcholine receptors regulate long-term potentiation at hippocampal CA3 pyramidal cell synapses in an input-specific fashion.Journal of neurophysiology · 2012Article
- Consequences of inhibiting amyloid precursor protein processing enzymes on synaptic function and plasticity.Neural plasticity · 2012Review
- Pathway-specific alteration of synaptic plasticity in Tg2576 mice.Molecules and cells · 2011Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
β-Site amyloid precursor protein-cleaving enzyme 1 (BACE1)-the neuronal β-secretase responsible for producing β-amyloid (Aβ) peptides-emerged as one of the key therapeutic targets of Alzheimer's disease (AD). Although complete ablation of the BACE1 gene prevents Aβ formation, we reported that BACE1 knock-out mice display severe presynaptic deficits at mossy fiber (MF)-to-CA3 synapses in the hippocampus, a major locus of BACE1 expression. We also found that the deficits are likely due to abnormal presynaptic Ca(2+) regulation. Cholinergic system has been implicated in AD, in some cases involving Ca(2+)-permeable α7-nicotinic acetylcholine receptors (nAChRs). Here we report that brief application of nicotine, via α7-nAChRs, can restore MF long-term potentiation in BACE1 knock-outs. Our data suggest that activating α7-nAChRs can recover the presynaptic deficits in BACE1 knock-outs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.