ArticleMolecular pain
Nerve injury elevates functional Cav3.2 channels in superficial spinal dorsal horn.
Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 67 citations in OpenAlex.
- A pathological missense mutation in the deubiquitinase USP5 leads to insensitivity to pain.The Journal of experimental medicine · 2025Article
- Fucoxanthin Inhibits the NMDA and AMPA Receptors Through Regulating the Calcium Response on Substantia Gelatinosa Neurons of the Trigeminal Subnucleus Caudalis in Juvenile Mice.Neural plasticity · 2025Article
- Regulatory Action of Calcium and Calcium Channels in Pain Pathways.International journal of biological sciences · 2025Review
- Stem cell exosome-loaded Gelfoam improves locomotor dysfunction and neuropathic pain in a rat model of spinal cord injury.Stem cell research & therapy · 2024Article
- A novel approach to completely alleviate peripheral neuropathic pain in human patients: insights from preclinical data.Frontiers in neuroanatomy · 2024Review
- Cav3.2 T-Type calcium channels downregulation attenuates bone cancer pain induced by inhibiting IGF-1/HIF-1α signaling pathway in the rat spinal cord.Journal of bone oncology · 2023Article
- T-type calcium channel modulation by hydrogen sulfide in neuropathic pain conditions.Frontiers in pharmacology · 2023Review
- Unveiling the mechanisms of neuropathic pain suppression: perineural resiniferatoxin targets Trpv1 and beyond.Frontiers in neuroanatomy · 2023Article
- T-Type Calcium Channels: A Mixed Blessing.International journal of molecular sciences · 2022Review
- Central and peripheral contributions of T-type calcium channels in pain.Molecular brain · 2022Review
- [Effects ofBeijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2022Article
- Voltage-dependent CaPflugers Archiv : European journal of physiology · 2022Review
- Shared nociceptive dorsal root ganglion neurons participating in acupoint sensitization.Frontiers in molecular neuroscience · 2022Article
- The Mechanisms of Plasticity of Nociceptive Ion Channels in Painful Diabetic Neuropathy.Frontiers in pain research (Lausanne, Switzerland) · 2022Review
- The T-Type Calcium Channel Cav3.2 in Somatostatin Interneurons in Spinal Dorsal Horn Participates in Mechanosensation and Mechanical Allodynia in Mice.Frontiers in cellular neuroscience · 2022Article
- Genetic Deficiency of p53 Leads to Structural, Functional, and Synaptic Deficits in Primary Somatosensory Cortical Neurons of Adult Mice.Frontiers in molecular neuroscience · 2022Article
- Painful diabetic neuropathy leads to functional CaExperimental neurology · 2021Article
- Article
- The T-type calcium channel antagonist, Z944, reduces spinal excitability and pain hypersensitivity.British journal of pharmacology · 2021Article
- Targeting T-type/CaV3.2 channels for chronic pain.Translational research : the journal of laboratory and clinical medicine · 2021Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cav3 channels play an important role in modulating chronic pain. However, less is known about the functional changes of Cav3 channels in superficial spinal dorsal horn in neuropathic pain states. Here, we examined the effect of partial sciatic nerve ligation (PSNL) on either expression or electrophysiological properties of Cav3 channels in superficial spinal dorsal horn. Our in vivo studies showed that the blockers of Cav3 channels robustly alleviated PSNL-induced mechanical allodynia and thermal hyperalgesia, which lasted at least 14 days following PSNL. Meanwhile, PSNL triggered an increase in both mRNA and protein levels of Cav3.2 but not Cav3.1 or Cav3.3 in rats. However, in Cav3.2 knockout mice, PSNL predominantly attenuated mechanical allodynia but not thermal hyperalgesia. In addition, the results of whole-cell patch-clamp recordings showed that both the overall proportion of Cav3 current-expressing neurons and the Cav3 current density in individual neurons were elevated in spinal lamina II neurons from PSNL rats, which could not be recapitulated in Cav3.2 knockout mice. Altogether, our findings reveal that the elevated functional Cav3.2 channels in superficial spinal dorsal horn may contribute to the mechanical allodynia in PSNL-induced neuropathic pain model.
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