ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
The active zone protein family ELKS supports Ca2+ influx at nerve terminals of inhibitory hippocampal neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
52 citing papers in PubMed, 82 citations in OpenAlex.
- Article
- Deployment of endocytic machinery to periactive zones of nerve terminals is independent of active zone assembly and evoked release.bioRxiv : the preprint server for biology · 2026Article
- Role of tRNA-Derived Fragments and Their Modifications in the Pathogenesis and Treatment of Alzheimer's Disease.Molecular neurobiology · 2025Review
- On the targeting of voltage-gated calcium channels to neurotransmitter release sites.Current opinion in neurobiology · 2024Review
- CaeLife · 2024Article
- Distinct active zone protein machineries mediate CaNature neuroscience · 2024Article
- The intracellular C-terminus confers compartment-specific targeting of voltage-gated calcium channels.Cell reports · 2024Article
- CabioRxiv : the preprint server for biology · 2024Article
- Mapping proteomic composition of excitatory postsynaptic sites in the cerebellar cortex.Frontiers in molecular neuroscience · 2024Article
- The intracellular C-terminus confers compartment-specific targeting of voltage-gated CabioRxiv : the preprint server for biology · 2023Article
- Molecular definition of distinct active zone protein machineries for CabioRxiv : the preprint server for biology · 2023Article
- Interactive nanocluster compaction of the ELKS scaffold and Cacophony CaScience advances · 2023Article
- Article
- Munc13 supports fusogenicity of non-docked vesicles at synapses with disrupted active zones.eLife · 2022Article
- Structure and Function of the Mammalian Neuromuscular Junction.Comprehensive Physiology · 2022Article
- Article
- Organization and dynamics of the cortical complexes controlling insulin secretion in β-cells.Journal of cell science · 2022Article
- Similarity and Diversity of Presynaptic Molecules at Neuromuscular Junctions and Central Synapses.Biomolecules · 2022Review
- Diverse organization of voltage-gated calcium channels at presynaptic active zones.Frontiers in synaptic neuroscience · 2022Review
- Mechanisms controlling the trafficking, localization, and abundance of presynaptic CaFrontiers in molecular neuroscience · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
In a presynaptic nerve terminal, synaptic vesicle exocytosis is restricted to specialized sites called active zones. At these sites, neurotransmitter release is determined by the number of releasable vesicles and their probability of release. Proteins at the active zone set these parameters by controlling the presynaptic Ca(2+) signal, and through docking and priming of synaptic vesicles. Vertebrate ELKS proteins are enriched at presynaptic active zones, but their functions are not well understood. ELKS proteins are produced by two genes in vertebrates, and each gene contributes ∼50% to total brain ELKS. We generated knock-out mice for ELKS1 and found that its constitutive removal causes lethality. To bypass lethality, and to circumvent redundancy between ELKS1 and ELKS2 in synaptic transmission, we used a conditional genetic approach to remove both genes in cultured hippocampal neurons after synapses are established. Simultaneous removal of ELKS1 and ELKS2 resulted in a 50% decrease of neurotransmitter release at inhibitory synapses, paralleled by a reduction in release probability. Removal of ELKS did not affect synapse numbers or their electron microscopic appearance. Using Ca(2+) imaging, we found that loss of ELKS caused a 30% reduction in single action potential-triggered Ca(2+) influx in inhibitory nerve terminals, consistent with the deficits in synaptic transmission and release probability. Unlike deletion of the active zone proteins RIM, RIM-BP, or bruchpilot, ELKS removal did not lead to a measurable reduction in presynaptic Ca(2+) channel levels. Our results reveal that ELKS is required for normal Ca(2+) influx at nerve terminals of inhibitory hippocampal neurons.
Indexed as
Identifiers
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.