ReviewFrontiers in cellular neuroscience2014
How voltage-gated calcium channels gate forms of homeostatic synaptic plasticity.
Review in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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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.
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Who cites it
39 citing papers in PubMed, 57 citations in OpenAlex.
- Reduced MOV10 reveals novel functional cortical connections in an increased fear response.bioRxiv : the preprint server for biology · 2026Article
- Common themes in evoked ion channel translocation in neuroplastic and homeostatic plasticity.Frontiers in pharmacology · 2026Review
- Postnatal development of electrophysiological and morphological properties in layer 2/3 and layer 5 pyramidal neurons in the mouse primary visual cortex.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Human iPSC-Derived Cortical Neurons Display Homeostatic Plasticity.Life (Basel, Switzerland) · 2022Article
- Potentials of Neuropeptides as Therapeutic Agents for Neurological Diseases.Biomedicines · 2022Review
- Mechanisms controlling the trafficking, localization, and abundance of presynaptic CaFrontiers in molecular neuroscience · 2022Review
- Crosstalk Between GABAergic Neurotransmission and Inflammatory Cascades in the Post-ischemic Brain: Relevance for Stroke Recovery.Frontiers in cellular neuroscience · 2022Review
- The calcineurin regulator Sarah enables distinct forms of homeostatic plasticity at theFrontiers in synaptic neuroscience · 2022Article
- Homeostatic plasticity and burst activity are mediated by hyperpolarization-activated cation currents and T-type calcium channels in neuronal cultures.Scientific reports · 2021Article
- Homeostatic Depression Shows Heightened Sensitivity to Synaptic Calcium.Frontiers in cellular neuroscience · 2021Article
- Contribution of D1R-expressing neurons of the dorsal dentate gyrus and CaNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Homeostatic control of Drosophila neuromuscular junction function.Synapse (New York, N.Y.) · 2020Review
- Gain-of-function mutations in the UNC-2/CaV2α channel lead to excitation-dominant synaptic transmission ineLife · 2019Article
- Maintenance of homeostatic plasticity at theeLife · 2019Article
- Up-regulation of CaMolecular and cellular biochemistry · 2018Article
- Drosophila CaV2 channels harboring human migraine mutations cause synapse hyperexcitability that can be suppressed by inhibition of a Ca2+ store release pathway.PLoS genetics · 2018Article
- Homeostatic Presynaptic Plasticity Is Specifically Regulated by P/Q-type CaCell reports · 2017Article
- Restoration of Motor Defects Caused by Loss ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- From Gene to Behavior: L-Type Calcium Channel Mechanisms Underlying Neuropsychiatric Symptoms.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017Review
- A microRNA-129-5p/Rbfox crosstalk coordinates homeostatic downscaling of excitatory synapses.The EMBO journal · 2017Article
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1 author at 1 institution in 1 country.
Funding
Abstract
Throughout life, animals face a variety of challenges such as developmental growth, the presence of toxins, or changes in temperature. Neuronal circuits and synapses respond to challenges by executing an array of neuroplasticity paradigms. Some paradigms allow neurons to up- or downregulate activity outputs, while countervailing ones ensure that outputs remain within appropriate physiological ranges. A growing body of evidence suggests that homeostatic synaptic plasticity (HSP) is critical in the latter case. Voltage-gated calcium channels gate forms of HSP. Presynaptically, the aggregate data show that when synapse activity is weakened, homeostatic signaling systems can act to correct impairments, in part by increasing calcium influx through presynaptic CaV2-type channels. Increased calcium influx is often accompanied by parallel increases in the size of active zones and the size of the readily releasable pool of presynaptic vesicles. These changes coincide with homeostatic enhancements of neurotransmitter release. Postsynaptically, there is a great deal of evidence that reduced network activity and loss of calcium influx through CaV1-type calcium channels also results in adaptive homeostatic signaling. Some adaptations drive presynaptic enhancements of vesicle pool size and turnover rate via retrograde signaling, as well as de novo insertion of postsynaptic neurotransmitter receptors. Enhanced calcium influx through CaV1 after network activation or single cell stimulation can elicit the opposite response-homeostatic depression via removal of excitatory receptors. There exist intriguing links between HSP and calcium channelopathies-such as forms of epilepsy, migraine, ataxia, and myasthenia. The episodic nature of some of these disorders suggests alternating periods of stable and unstable function. Uncovering information about how calcium channels are regulated in the context of HSP could be relevant toward understanding these and other disorders.
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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.