ELKS2α/CAST deletion selectively increases neurotransmitter release at inhibitory synapses
Open accessAbstract
The presynaptic active zone is composed of a protein network that contains ELKS2alpha (a.k.a. CAST) as a central component. Here we demonstrate that in mice, deletion of ELKS2alpha caused a large increase in inhibitory, but not excitatory, neurotransmitter release, and potentiated the size, but not the properties, of the readily-releasable pool of vesicles at inhibitory synapses. Quantitative electron microscopy revealed that the ELKS2alpha deletion did not change the number of docked vesicles or other ultrastructural parameters of synapses, except for a small decrease in synaptic vesicle numbers. The ELKS2alpha deletion did, however, alter the excitatory/inhibitory balance and exploratory behaviors, possibly as a result of the increased synaptic inhibition. Thus, as opposed to previous studies indicating that ELKS2alpha is essential for mediating neurotransmitter release, our results suggest that ELKS2alpha normally restricts release and limits the size of the readily-releasable pool of synaptic vesicles at the active zone of inhibitory synapses.
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Acute or constitutive deletion of ELKS2 in mice caused an increase in the readily releasable pool of synaptic vesicles.
“although acute or constitutive deletion of ELKS2 in mice did not produce a decrease in neurotransmitter release, they caused an increase in the readily releasable pool of synaptic vesicles (Kaeser et al., 2009).”
From The Presynaptic Active Zone (2012) · cites this paper as Kaeser et al., 2009
The Introduction and Results report that ELKS2α deletion did not impair release and increased the readily releasable pool, but specify that the increase occurred at inhibitory synapses; the Results report no RRP change at excitatory synapses. The RRP was measured directly after conditional deletion in cultured neurons, while constitutive knockout mice showed increased inhibitory transmission. The citing sentence omits the synapse-specific qualifier and implies the RRP increase was demonstrated directly for both deletion approaches. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMammalian ELKS genes contain alternative N-terminal promoters and alternatively spliced C-terminal sequences, with a shorter C-terminal sequence that is primarily expressed in brain and a longer C-terminal sequence that is primarily expressed in peripheral tissues.
“Mammalian ELKS genes contain alternative N-terminal promoters and alternatively spliced C-terminal sequences, with a shorter C-terminal sequence that is primarily expressed in brain and a longer C-terminal sequence that is primarily expressed in peripheral tissues (Wang et al., 2002; Kaeser et al., 2009).”
From The Presynaptic Active Zone (2012) · cites this paper as Kaeser et al., 2009
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Experimental — accuracy not yet measuredDeletion of ELKS in C. elegans and of ELKS2 in mice did not impair neurotransmitter release.
“deletion of ELKS in C. elegans and of ELKS2 in mice did not impair neurotransmitter release (Deken et al., 2005; Kaeser et al., 2009).”
From The Presynaptic Active Zone (2012) · cites this paper as Kaeser et al., 2009
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Cites
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Self-citation
- Authors
- Kaeser, P. S., Deng, L., Chávez, A. E., Liu, X., Castillo, P. E., & Südhof, T. C.
- Affiliations
- Stanford Medicine (US)
- Albert Einstein College of Medicine (US)
- The University of Texas Southwestern Medical Center (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Südhof, Thomas C.
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2009-10
- Volume
- 64
- Issue
- 2
- Pages
- 227-239
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC2785857
- OpenAlex
- W2006184695
- Cited by
- 102
- References
- 7
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 2 · 2023: 2 · 2022: 11 · 2021: 4 · 2020: 9 · 2019: 4 · 2018: 6 · 2017: 8 · 2016: 7 · 2015: 7 · 2014: 6 · 2013: 5 · 2012: 8
- FWCI
- 3.26
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1385 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Alliance for Research on Schizophrenia and Depression
- National Institutes of Health
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- National Institute of Neurological Disorders and Stroke (33564, DA17392)
- Irma T. Hirschl Trust
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- CAST, active zone, readily releasable vesicles, synaptic vesicle pools, excitation-inhibition balance, synaptic inhibition, docked vesicles, synaptic ultrastructure, exploratory behavior, knockout mice
- MeSH terms
- Animals, Animals, Newborn, Behavior, Animal, Brain, Calcium, Carrier Proteins, Cells, Cultured, Electric Stimulation, Hippocampus, Models, Neurological, Movement, Nerve Tissue Proteins, Neurons, Synapses, Synaptosomes, Gene Deletion, Mice, Knockout, Neurotransmitter Agents, Patch-Clamp Techniques, GTP-Binding Proteins, Protein Isoforms, rab GTP-Binding Proteins, Microscopy, Electron, Transmission, Green Fluorescent Proteins, Mice, Inhibitory Postsynaptic Potentials, In Vitro Techniques
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