ArticleNeuroscience2007
Increased asynchronous release and aberrant calcium channel activation in amyloid precursor protein deficient neuromuscular synapses.
Article in Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 51 citations in OpenAlex.
- Nanomolar Cadmium Disrupts Neurotransmitter Release Timing via a ROS-dependent Mechanism at the Mouse Neuromuscular Junction: Modulation by Nanomolar ZnNeurochemical research · 2026Article
- Impact of distinct neurotransmitter release modes on neuronal signaling.Molecular psychiatry · 2026Review
- L-type CaCellular and molecular neurobiology · 2022Article
- Presynaptic Acetylcholine Receptors Modulate the Time Course of Action Potential-Evoked Acetylcholine Quanta Secretion at Neuromuscular Junctions.Biomedicines · 2022Review
- Upregulated CaCells · 2022Article
- Lack of APLP1 leads to subtle alterations in neuronal morphology but does not affect learning and memory.Frontiers in molecular neuroscience · 2022Article
- Fe65: A Scaffolding Protein of Actin Regulators.Cells · 2021Review
- The physiological role of α-synuclein and its relationship to Parkinson's Disease.Journal of neurochemistry · 2019Review
- Mechanism of P2X7 receptor-dependent enhancement of neuromuscular transmission in pannexin 1 knockout mice.Purinergic signalling · 2018Article
- Pre-clinical symptoms of SBMA may not be androgen-dependent: implications from two SBMA mouse models.Human molecular genetics · 2018Article
- Not just amyloid: physiological functions of the amyloid precursor protein family.Nature reviews. Neuroscience · 2017Review
- Article
- Defects in Neuromuscular Transmission May Underlie Motor Dysfunction in Spinal and Bulbar Muscular Atrophy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Signaling pathways regulating neuron-glia interaction and their implications in Alzheimer's disease.Journal of neurochemistry · 2016Review
- The HERC1 E3 Ubiquitin Ligase is essential for normal development and for neurotransmission at the mouse neuromuscular junction.Cellular and molecular life sciences : CMLS · 2015Article
- More than cholesterol transporters: lipoprotein receptors in CNS function and neurodegeneration.Neuron · 2014Review
- Molecular mechanisms for synchronous, asynchronous, and spontaneous neurotransmitter release.Annual review of physiology · 2014Review
- Tyr682 in the Aβ-precursor protein intracellular domain regulates synaptic connectivity, cholinergic function, and cognitive performance.Aging cell · 2012Article
- Proteomic analysis of the presynaptic active zone.Experimental brain research · 2012Review
- Physiological functions of APP family proteins.Cold Spring Harbor perspectives in medicine · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Despite the critical roles of the amyloid precursor protein (APP) in Alzheimer's disease pathogenesis, its physiological function remains poorly established. Our previous studies implicated a structural and functional activity of the APP family of proteins in the developing neuromuscular junction (NMJ). Here we performed comprehensive analyses of neurotransmission in mature neuromuscular synapse of APP deficient mice. We found that APP deletion led to reduced paired-pulse facilitation and increased depression of synaptic transmission with repetitive stimulation. Readily releasable pool size and total releasable vesicles were not affected, but probability of release was significantly increased. Strikingly, the amount of asynchronous release, a measure sensitive to presynaptic calcium concentration, was dramatically increased, and pharmacological studies revealed that it was attributed to aberrant activation of N- and L-type Ca(2+) channels. We propose that APP modulates synaptic transmission at the NMJ by ensuring proper Ca(2+) channel function.
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What OpenQuestion holds
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.