ArticleJournal of neurochemistry2011
Diabetic neuropathy enhances voltage-activated Ca2+ channel activity and its control by M4 muscarinic receptors in primary sensory neurons.
Article in Journal of neurochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- Targeting Spinal Dorsal Horn Sensitisation in Chronic Pain: Mechanisms and Translational Strategies.Neuroscience bulletin · 2026Review
- Diabetic impact on the neuroaxis: from peripheral neuropathy to central neurodegeneration.Frontiers in endocrinology · 2026Review
- Peripheral Parasympathetic Networks in Pain: A Systems-Level Review of Mechanisms and Modulations.Cellular and molecular neurobiology · 2025Review
- Spinal neuron-glial crosstalk and ion channel dysregulation in diabetic neuropathic pain.Frontiers in immunology · 2025Review
- Diabetes-Induced Amplification of Nociceptive DRG Neuron Output by Upregulation of Somatic T-Type CaBiomolecules · 2023Article
- Painful diabetic neuropathy leads to functional CaExperimental neurology · 2021Article
- Alpha lipoic acid attenuates evoked and spontaneous pain following surgical skin incision in rats.Channels (Austin, Tex.) · 2021Article
- Pathophysiological roles and therapeutic potential of voltage-gated ion channels (VGICs) in pain associated with herpesvirus infection.Cell & bioscience · 2020Review
- Cortex Mori Radicis extract promotes neurite outgrowth in diabetic rats by activating PI3K/AKT signaling and inhibiting Ca2+ influx associated with the upregulation of transient receptor potential canonical channel 1.Molecular medicine reports · 2020Article
- Streptozotocin-Induced Diabetic Neuropathic Pain Is Associated with Potentiated Calcium-Permeable AMPA Receptor Activity in the Spinal Cord.The Journal of pharmacology and experimental therapeutics · 2019Article
- Analgesic transient receptor potential vanilloid-1-active compounds inhibit native and recombinant T-type calcium channels.British journal of pharmacology · 2019Article
- 5-Oxo-hexahydroquinoline: an attractive scaffold with diverse biological activities.Molecular diversity · 2019Review
- Molecular, Cellular and Circuit Basis of Cholinergic Modulation of Pain.Neuroscience · 2018Review
- Recent advances in the development of T-type calcium channel blockers for pain intervention.British journal of pharmacology · 2018Review
- miR-9 Mediates CALHM1-Activated ATP-P2X7R Signal in Painful Diabetic Neuropathy Rats.Molecular neurobiology · 2017Article
- Cholinergic Nociceptive Mechanisms in Rat Meninges and Trigeminal Ganglia: Potential Implications for Migraine Pain.Frontiers in neurology · 2017Article
- Muscarinic receptor subtypes differentially control synaptic input and excitability of cerebellum-projecting medial vestibular nucleus neurons.Journal of neurochemistry · 2016Article
- Two heterozygous Cav3.2 channel mutations in a pediatric chronic pain patient: recording condition-dependent biophysical effects.Pflugers Archiv : European journal of physiology · 2016Article
- Effect of the T-type channel blocker KYS-05090S in mouse models of acute and neuropathic pain.Pflugers Archiv : European journal of physiology · 2016Article
- Modulation of Cav3.2 T-type calcium channel permeability by asparagine-linked glycosylation.Channels (Austin, Tex.) · 2016Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Painful neuropathy is one of the most serious complications of diabetes and remains difficult to treat. The muscarinic acetylcholine receptor (mAChR) agonists have a profound analgesic effect on painful diabetic neuropathy. Here we determined changes in T-type and high voltage-activated Ca(2+) channels (HVACCs) and their regulation by mAChRs in dorsal root ganglion (DRG) neurons in a rat model of diabetic neuropathy. The HVACC currents in large neurons, T-type currents in medium and large neurons, the percentage of small DRG neurons with T-type currents, and the Cav3.2 mRNA level were significantly increased in diabetic rats compared with those in control rats. The mAChR agonist oxotremorine-M significantly inhibited HVACCs in a greater proportion of DRG neurons with and without T-type currents in diabetic than in control rats. In contrast, oxotremorine-M had no effect on HVACCs in small and large neurons with T-type currents and in most medium neurons with T-type currents from control rats. The M(2) and M(4) antagonist himbacine abolished the effect of oxotremorine-M on HVACCs in both groups. The selective M(4) antagonist muscarinic toxin-3 caused a greater attenuation of the effect of oxotremorine-M on HVACCs in small and medium DRG neurons in diabetic than in control rats. Additionally, the mRNA and protein levels of M(4), but not M(2), in the DRG were significantly greater in diabetic than in control rats. Our findings suggest that diabetic neuropathy potentiates the activity of T-type and HVACCs in primary sensory neurons. M(4) mAChRs are up-regulated in DRG neurons and probably account for increased muscarinic analgesic effects in diabetic neuropathic pain.
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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.