ArticleThe Journal of physiology2014
Native store-operated calcium channels are functionally expressed in mouse spinal cord dorsal horn neurons and regulate resting calcium homeostasis.
Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- STIM-Orai signaling in neurons: integrating calcium dynamics and synaptic plasticity.Cell communication and signaling : CCS · 2026Review
- BTP2, a store-operated calcium channel inhibitor, attenuates morphine antinociceptive tolerance in rats.Frontiers in neuroscience · 2026Article
- STIM1 functionally couples to transient receptor potential ankyrin 1 contributing to nociception.Pain · 2025Article
- STIM Proteins: The Gas and Brake of Calcium Entry in Neurons.Neuroscience bulletin · 2025Review
- PGE2 Potentiates Orai1-Mediated Calcium Entry Contributing to Peripheral Sensitization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Store-operated calcium entry mediates hyperalgesic responses during neuropathy.FEBS open bio · 2023Article
- Neuronal Store-Operated Calcium Channels.Molecular neurobiology · 2023Review
- SKF96365 impedes spinal glutamatergic transmission-mediated neuropathic allodynia.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- Estrogen receptors in pain modulation: cellular signaling.Biology of sex differences · 2021Review
- Store-Operated Calcium Channels in Physiological and Pathological States of the Nervous System.Frontiers in cellular neuroscience · 2020Review
- Calcium Deregulation and Mitochondrial Bioenergetics in GDAP1-Related CMT Disease.International journal of molecular sciences · 2019Review
- Calcium release-activated calcium channels and pain.Cell calcium · 2018Review
- Presenilin-1 Delta E9 Mutant Induces STIM1-Driven Store-Operated Calcium Channel Hyperactivation in Hippocampal Neurons.Molecular neurobiology · 2018Article
- Orai1 Plays a Crucial Role in Central Sensitization by Modulating Neuronal Excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Neuronal P2X7 receptor-induced reactive oxygen species production contributes to nociceptive behavior in mice.Scientific reports · 2017Article
- Role of STIM2 in cell function and physiopathology.The Journal of physiology · 2017Review
- Minoxidil is a potential neuroprotective drug for paclitaxel-induced peripheral neuropathy.Scientific reports · 2017Article
- Sexual Dimorphism in a Reciprocal Interaction of Ryanodine and IPThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Orai1 and Orai3 Mediate Store-Operated Calcium Entry Contributing to Neuronal Excitability in Dorsal Root Ganglion Neurons.Frontiers in cellular neuroscience · 2017Article
- Store-Operated Calcium Entry Is Required for mGluR-Dependent Long Term Depression in Cortical Neurons.Frontiers in cellular neuroscience · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
Store-operated calcium channels (SOCs) are calcium-selective cation channels that mediate calcium entry in many different cell types. Store-operated calcium entry (SOCE) is involved in various cellular functions. Increasing evidence suggests that impairment of SOCE is responsible for numerous disorders. A previous study demonstrated that YM-58483, a potent SOC inhibitor, strongly attenuates chronic pain by systemic or intrathecal injection and completely blocks the second phase of formalin-induced spontaneous nocifensive behaviour, suggesting a potential role of SOCs in central sensitization. However, the expression of SOCs, their molecular identity and function in spinal cord dorsal horn neurons remain elusive. Here, we demonstrate that SOCs are expressed in dorsal horn neurons. Depletion of calcium stores from the endoplasmic reticulum (ER) induced large sustained calcium entry, which was blocked by SOC inhibitors, but not by voltage-gated calcium channel blockers. Depletion of ER calcium stores activated inward calcium-selective currents, which was reduced by replacing Ca(2+) with Ba(2+) and reversed by SOC inhibitors. Using the small inhibitory RNA knockdown approach, we identified both STIM1 and STIM2 as important mediators of SOCE and SOC current, and Orai1 as a key component of the Ca(2+) release-activated Ca(2+) channels in dorsal horn neurons. Knockdown of STIM1, STIM2 or Orai1 decreased resting Ca(2+) levels. We also found that activation of neurokinin 1 receptors led to SOCE and activation of SOCs produced an excitatory action in dorsal horn neurons. Our findings reveal that a novel SOC signal is present in dorsal horn neurons and may play an important role in pain transmission.
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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.