ArticleThe Journal of physiology2012
Opioid-related (ORL1) receptors are enriched in a subpopulation of sensory neurons and prolonged activation produces no functional loss of surface N-type calcium channels.
Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Functional crosstalk between neuropeptide FF system and N-type voltage-gated calcium channels in ziconotide-mediated antinociception in mice.Psychopharmacology · 2026Article
- Molecular Anatomy of Synaptic and Extrasynaptic Neurotransmission Between Nociceptive Primary Afferents and Spinal Dorsal Horn Neurons.International journal of molecular sciences · 2025Review
- Regulation of Presynaptic Calcium Channels.Advances in neurobiology · 2023Article
- Regulation of N-type calcium channels by nociceptin receptors and its possible role in neurological disorders.Molecular brain · 2022Review
- A Crosstalk between the Cannabinoid Receptors and Nociceptin Receptors in Colitis-Clinical Implications.Journal of clinical medicine · 2022Review
- Knock-In Mouse Models to Investigate the Functions of Opioid ReceptorsFrontiers in cellular neuroscience · 2022Review
- Role of nociceptin/orphanin FQ and nociceptin opioid peptide receptor in depression and antidepressant effects of nociceptin opioid peptide receptor antagonists.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2019Review
- Modulation of Ion Channels in the Axon: Mechanisms and Function.Frontiers in cellular neuroscience · 2019Review
- The tarantula toxin β/δ-TRTX-Pre1a highlights the importance of the S1-S2 voltage-sensor region for sodium channel subtype selectivity.Scientific reports · 2017Article
- Pharmacological characterisation of the highly NaScientific reports · 2017Article
- Nociceptin/Orphanin FQ Receptor Structure, Signaling, Ligands, Functions, and Interactions with Opioid Systems.Pharmacological reviews · 2016Review
- Molecular Basis of Regulating High Voltage-Activated Calcium Channels by S-Nitrosylation.The Journal of biological chemistry · 2015Article
- Knock-In Mice with NOP-eGFP Receptors Identify Receptor Cellular and Regional Localization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Functional plasticity of the N/OFQ-NOP receptor system determines analgesic properties of NOP receptor agonists.British journal of pharmacology · 2014Review
- Novel ω-conotoxins from C. catus reverse signs of mouse inflammatory pain after systemic administration.Molecular pain · 2013Article
- Spinal actions of ω-conotoxins, CVID, MVIIA and related peptides in a rat neuropathic pain model.British journal of pharmacology · 2013Article
- Regulation of Ca(V)2 calcium channels by G protein coupled receptors.Biochimica et biophysica acta · 2013Review
- Cellular mechanisms of nociceptin/orphanin FQ (N/OFQ) peptide (NOP) receptor regulation and heterologous regulation by N/OFQ.Molecular pharmacology · 2013Review
- Serine 363 is required for nociceptin/orphanin FQ opioid receptor (NOPR) desensitization, internalization, and arrestin signaling.The Journal of biological chemistry · 2012Article
- γ-Aminobutyric acid type B (GABAB) receptor expression is needed for inhibition of N-type (Cav2.2) calcium channels by analgesic α-conotoxins.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The opioid-related receptor, ORL1, is activated by the neuropeptide nociceptin/orphanin FQ (N/OFQ) and inhibits high-voltage-activated (HVA) calcium channel currents (I(Ca)) via a G-protein-coupled mechanism. Endocytosis of ORL1 receptor during prolonged N/OFQ exposure was proposed to cause N-type voltage-gated calcium channel (VGCC) internalization via physical interaction between ORL1 and the N-type channel. However, there is no direct electrophysiological evidence for this mechanism in dorsal root ganglion (DRG) neurons or their central nerve terminals. The present study tested this using whole-cell patch-clamp recordings of HVA I(Ca) in rat DRG neurons and primary afferent excitatory synaptic currents (eEPSCs) in spinal cord slices. DRG neurons were classified on the basis of diameter, isolectin-B4 (IB4) binding and responses to capsaicin, N/OFQ and a μ-opioid agonist, DAMGO. IB4-negative neurons less than 20 μm diameter were selectively responsive to N/OFQ as well as DAMGO. In these neurons, ORL1 desensitization by a supramaximal concentration of N/OFQ was not followed by a decrease in HVA I(Ca) current density or proportion of whole-cell HVA I(Ca) contributed by N-type VGCC as determined using the N-type channel selective blocker, ω-conotoxin CVID. There was also no decrease in the proportion of N-type I(Ca) when neurons were incubated at 37°C with N/OFQ for 30 min prior to recording. In spinal cord slices, N/OFQ consistently inhibited eEPSCs onto dorsal horn neurons. As observed in DRG neurons, preincubation of slices in N/OFQ for 30 min produced no decrease in the proportion of eEPSCs inhibited by CVID. In conclusion, no internalization of the N-type VGCC occurs in either the soma or central nerve terminals of DRG neurons following prolonged exposure to high, desensitizing concentrations of N/OFQ.
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