ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
The upregulation of α2δ-1 subunit modulates activity-dependent Ca2+ signals in sensory neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 51 citations in OpenAlex.
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- Functional remodeling of presynaptic voltage-gated calcium channels in superficial layers of the dorsal horn during neuropathic pain.iScience · 2024Article
- Evaluation ofACS chemical neuroscience · 2023Article
- Voltage-gated calcium channel subunit αFrontiers in molecular neuroscience · 2023Article
- Role of α2δ-3 in regulating calcium channel localization at presynaptic active zones during homeostatic plasticity.Frontiers in molecular neuroscience · 2023Article
- Development of a PET radioligand for α2δ-1 subunit of calcium channels for imaging neuropathic pain.European journal of medicinal chemistry · 2022Article
- Depleted Calcium Stores and Increased Calcium Entry in Rod Photoreceptors of theInternational journal of molecular sciences · 2022Article
- Targeting Neuroimmune Interactions in Diabetic Neuropathy with Nanomedicine.Antioxidants & redox signaling · 2022Article
- The nAChR Chaperone TMEM35a (NACHO) Contributes to the Development of Hyperalgesia in Mice.Neuroscience · 2021Article
- Estrogen receptors in pain modulation: cellular signaling.Biology of sex differences · 2021Review
- Mirogabalin-A Novel Selective Ligand for the α2δ Calcium Channel Subunit.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Cannabinoid Therapeutics in Chronic Neuropathic Pain: From Animal Research to Human Treatment.Frontiers in physiology · 2021Review
- Mirogabalin: could it be the next generation gabapentin or pregabalin?The Korean journal of pain · 2021Review
- Different functions of two putative Drosophila αScientific reports · 2020Article
- Mitochondrial-Protective Effects of R-Phenibut after Experimental Traumatic Brain Injury.Oxidative medicine and cellular longevity · 2020Article
- Dynamic CRMP2 Regulation of CaV2.2 in the Prefrontal Cortex Contributes to the Reinstatement of Cocaine Seeking.Molecular neurobiology · 2020Article
- The Secretomes of Painful Versus Nonpainful Human Schwannomatosis Tumor Cells Differentially Influence Sensory Neuron Gene Expression and Sensitivity.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
As auxiliary subunits of voltage-gated Ca(2+) channels, the α2δ proteins modulate membrane trafficking of the channels and their localization to specific presynaptic sites. Following nerve injury, upregulation of the α2δ-1 subunit in sensory dorsal root ganglion neurons contributes to the generation of chronic pain states; however, very little is known about the underlying molecular mechanisms. Here we show that the increased expression of α2δ-1 in rat sensory neurons leads to prolonged Ca(2+) responses evoked by membrane depolarization. This mechanism is coupled to CaV2.2 channel-mediated responses, as it is blocked by a ω-conotoxin GVIA application. Once initiated, the prolonged Ca(2+) transients are not dependent on extracellular Ca(2+) and do not require Ca(2+) release from the endoplasmic reticulum. The selective inhibition of mitochondrial Ca(2+) uptake demonstrates that α2δ-1-mediated prolonged Ca(2+) signals are buffered by mitochondria, preferentially activated by Ca(2+) influx through CaV2.2 channels. Thus, by controlling channel abundance at the plasma membrane, the α2δ-1 subunit has a major impact on the organization of depolarization-induced intracellular Ca(2+) signaling in dorsal root ganglion neurons.
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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.