ArticleProceedings of the National Academy of Sciences of the United States of America2016
Calcium sensor regulation of the CaV2.1 Ca2+ channel contributes to short-term synaptic plasticity in hippocampal neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
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- Astroglial modulation of synaptic function in the non-demyelinated cerebellar cortex is dependent on MyD88 signaling in a model of toxic demyelination.Journal of neuroinflammation · 2025Article
- Effect of semaglutide and empagliflozin on cognitive function and hippocampal phosphoproteomic in obese mice.Frontiers in pharmacology · 2023Article
- Hippocampal interlamellar cell-cell connectome that counts.Journal of cellular physiology · 2022Review
- Multiscale modeling of presynaptic dynamics from molecular to mesoscale.PLoS computational biology · 2022Article
- Environmental Enrichment Enhances CaInternational journal of molecular sciences · 2021Article
- Neuronal Plasticity: Neuronal Organization is Associated with Neurological Disorders.Journal of molecular neuroscience : MN · 2020Review
- Presynaptic Calcium Channel Open Probability and Changes in Calcium Influx Throughout the Action Potential Determined Using AP-Waveforms.Frontiers in synaptic neuroscience · 2020Article
- Autaptic Cultures: Methods and Applications.Frontiers in synaptic neuroscience · 2020Article
- Plasticity in striatal dopamine release is governed by release-independent depression and the dopamine transporter.Nature communications · 2019Article
- Current Understanding of the Role of Neuronal Calcium Sensor 1 in Neurological Disorders.Molecular neurobiology · 2019Review
- Presynaptic Calcium Channels.International journal of molecular sciences · 2019Review
- The Role of CaCell reports · 2019Article
- Allosteric regulators selectively prevent CaeLife · 2018Article
- Persistent but Labile Synaptic Plasticity at Excitatory Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Control of Excitation/Inhibition Balance in a Hippocampal Circuit by Calcium Sensor Protein Regulation of Presynaptic Calcium Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Transmitter release site organization can predict synaptic function at the neuromuscular junction.Journal of neurophysiology · 2018Article
- Review
- Millisecond CaProceedings of the Japan Academy. Series B, Physical and biological sciences · 2017Review
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Short-term synaptic plasticity is induced by calcium (Ca(2+)) accumulating in presynaptic nerve terminals during repetitive action potentials. Regulation of voltage-gated CaV2.1 Ca(2+) channels by Ca(2+) sensor proteins induces facilitation of Ca(2+) currents and synaptic facilitation in cultured neurons expressing exogenous CaV2.1 channels. However, it is unknown whether this mechanism contributes to facilitation in native synapses. We introduced the IM-AA mutation into the IQ-like motif (IM) of the Ca(2+) sensor binding site. This mutation does not alter voltage dependence or kinetics of CaV2.1 currents, or frequency or amplitude of spontaneous miniature excitatory postsynaptic currents (mEPSCs); however, synaptic facilitation is completely blocked in excitatory glutamatergic synapses in hippocampal autaptic cultures. In acutely prepared hippocampal slices, frequency and amplitude of mEPSCs and amplitudes of evoked EPSCs are unaltered. In contrast, short-term synaptic facilitation in response to paired stimuli is reduced by ∼ 50%. In the presence of EGTA-AM to prevent global increases in free Ca(2+), the IM-AA mutation completely blocks short-term synaptic facilitation, indicating that synaptic facilitation by brief, local increases in Ca(2+) is dependent upon regulation of CaV2.1 channels by Ca(2+) sensor proteins. In response to trains of action potentials, synaptic facilitation is reduced in IM-AA synapses in initial stimuli, consistent with results of paired-pulse experiments; however, synaptic depression is also delayed, resulting in sustained increases in amplitudes of later EPSCs during trains of 10 stimuli at 10-20 Hz. Evidently, regulation of CaV2.1 channels by CaS proteins is required for normal short-term plasticity and normal encoding of information in native hippocampal synapses.
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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.