ArticleThe Journal of biological chemistry2012
Up-regulation of Cavβ3 subunit in primary sensory neurons increases voltage-activated Ca2+ channel activity and nociceptive input in neuropathic pain.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- Regulation of stress susceptibility by chromatin-binding protein PHF6 in the pituitary intermediate lobe.Molecular psychiatry · 2026Article
- Dietary folic acid prevents peripheral neuropathy in mouse models of neural tube defects and type 2 diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Neuroplasticity in the transition from acute to chronic pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
- Functional remodeling of presynaptic voltage-gated calcium channels in superficial layers of the dorsal horn during neuropathic pain.iScience · 2024Article
- A peptidomimetic modulator of the CaProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Human-specific duplicate CHRFAM7A gene is associated with more severe osteoarthritis and amplifies pain behaviours.Annals of the rheumatic diseases · 2023Article
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- β subunits of voltage-gated calcium channels in cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Comparison of quinazoline and benzoylpyrazoline chemotypes targeting the CaVα-β interaction as antagonists of the N-type CaV2.2 channel.Channels (Austin, Tex.) · 2021Article
- Role of Micro-RNA for Pain After Surgery: Narrative Review of Animal and Human Studies.Anesthesia and analgesia · 2020Review
- Article
- Molecular Basis of Regulating High Voltage-Activated Calcium Channels by S-Nitrosylation.The Journal of biological chemistry · 2015Article
- Electrophysiological characterization of activation state-dependent Ca(v)2 channel antagonist TROX-1 in spinal nerve injured rats.Neuroscience · 2015Article
- Nerve injury induces a Gem-GTPase-dependent downregulation of P/Q-type Ca2+ channels contributing to neurite plasticity in dorsal root ganglion neurons.Pflugers Archiv : European journal of physiology · 2015Article
- Potentiation of high voltage-activated calcium channels by 4-aminopyridine depends on subunit composition.Molecular pharmacology · 2014Article
- Casein kinase II regulates N-methyl-D-aspartate receptor activity in spinal cords and pain hypersensitivity induced by nerve injury.The Journal of pharmacology and experimental therapeutics · 2014Article
- Epigenetic modification of DRG neuronal gene expression subsequent to nerve injury: etiological contribution to complex regional pain syndromes (Part II).Medical science monitor : international medical journal of experimental and clinical research · 2014Review
- Effects of arginine 10 to lysine substitution on ω-conotoxin CVIE and CVIF block of Cav2.2 channels.British journal of pharmacology · 2014Article
- Article
- An approach to identify microRNAs involved in neuropathic pain following a peripheral nerve injury.Frontiers in neuroscience · 2014Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
High voltage-activated calcium channels (HVACCs) are essential for synaptic and nociceptive transmission. Although blocking HVACCs can effectively reduce pain, this treatment strategy is associated with intolerable adverse effects. Neuronal HVACCs are typically composed of α(1), β (Cavβ), and α(2)δ subunits. The Cavβ subunit plays a crucial role in the membrane expression and gating properties of the pore-forming α(1) subunit. However, little is known about how nerve injury affects the expression and function of Cavβ subunits in primary sensory neurons. In this study, we found that Cavβ(3) and Cavβ(4) are the most prominent subtypes expressed in the rat dorsal root ganglion (DRG) and dorsal spinal cord. Spinal nerve ligation (SNL) in rats significantly increased mRNA and protein levels of the Cavβ(3), but not Cavβ(4), subunit in the DRG. SNL also significantly increased HVACC currents in small DRG neurons and monosynaptic excitatory postsynaptic currents of spinal dorsal horn neurons evoked from the dorsal root. Intrathecal injection of Cavβ(3)-specific siRNA significantly reduced HVACC currents in small DRG neurons and the amplitude of monosynaptic excitatory postsynaptic currents of dorsal horn neurons in SNL rats. Furthermore, intrathecal treatment with Cavβ(3)-specific siRNA normalized mechanical hyperalgesia and tactile allodynia caused by SNL but had no significant effect on the normal nociceptive threshold. Our findings provide novel evidence that increased expression of the Cavβ(3) subunit augments HVACC activity in primary sensory neurons and nociceptive input to dorsal horn neurons in neuropathic pain. Targeting the Cavβ(3) subunit at the spinal level represents an effective strategy for treating neuropathic pain.
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