ArticleEuropean journal of pain (London, England)2018
Allosteric modulation of α4β2* nicotinic acetylcholine receptors: Desformylflustrabromine potentiates antiallodynic response of nicotine in a mouse model of neuropathic pain.
Article in European journal of pain (London, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Nicotinic acetylcholine receptors in pain modulation.Frontiers in pharmacology · 2026Review
- α4β2The Journal of physiology · 2025Article
- Exploring Cholinergic Compounds for Peripheral Neuropathic Pain Management: A Comprehensive Scoping Review of Rodent Model Studies.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Persistent sensory changes and sex differences in transgenic mice conditionally expressing HIV-1 Tat regulatory protein.Experimental neurology · 2022Article
- Article
- Potentiation of (α4)2(β2)3, but not (α4)3(β2)2, nicotinic acetylcholine receptors reduces nicotine self-administration and withdrawal symptoms.Neuropharmacology · 2021Article
- Conditional expression of HIV-1 tat in the mouse alters the onset and progression of tonic, inflammatory and neuropathic hypersensitivity in a sex-dependent manner.European journal of pain (London, England) · 2020Article
- Allosterism of Nicotinic Acetylcholine Receptors: Therapeutic Potential for Neuroinflammation Underlying Brain Trauma and Degenerative Disorders.International journal of molecular sciences · 2020Review
- Examining the Effects of (α4)3(β2)2 Nicotinic Acetylcholine Receptor-Selective Positive Allosteric Modulator on Acute Thermal Nociception in Rats.Molecules (Basel, Switzerland) · 2020Article
- Desformylflustrabromine, a positive allosteric modulator of α4β2-containing nicotinic acetylcholine receptors, enhances cognition in rats.Pharmacological reports : PR · 2020Article
- Acute Administration of Desformylflustrabromine Relieves Chemically Induced Pain in CD-1 Mice.Molecules (Basel, Switzerland) · 2019Article
- Nicotine and sleep deprivation: impact on pain sensitivity and immune modulation in rats.Scientific reports · 2018Article
- Effect of nicotine and alpha-7 nicotinic modulators on visceral pain-induced conditioned place aversion in mice.European journal of pain (London, England) · 2018Article
- LY2087101 and dFBr share transmembrane binding sites in the (α4)3(β2)2 Nicotinic Acetylcholine Receptor.Scientific reports · 2018Article
- Nicotine Prevents and Reverses Paclitaxel-Induced Mechanical Allodynia in a Mouse Model of CIPN.The Journal of pharmacology and experimental therapeutics · 2018Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundNeuronal nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels. The α4β2 subtype of nAChRs plays an important role in the mediation of pain and several nicotine-evoked responses. Agonists and partial agonists of α4β2 nAChRs show efficacy in animal pain models. In addition, the antinociceptive properties of nicotine, a non-selective nAChR agonist with a high affinity for α4β2 nAChRs, is well-known. There is a growing body of evidence pointing to allosteric modulation of nAChRs as an alternative treatment strategy in experimental pain. Desformylflustrabromine (dFBr) is a positive allosteric modulator (PAM) at α4β2 nAChRs that enhances agonist responses without activating receptors. We hypothesized that dFBr may enhance nicotine-induced antinociception.
methodsThe present study investigated whether dFBr could attenuate mouse chronic constriction injury (CCI)-induced neuropathic pain by increasing endogenous cholinergic tone or potentiating the nicotine-evoked antiallodynic response.
resultsWe found that subcutaneous administration of dFBr failed to reduce pain behaviour on its own. However, the combination of dFBr with nicotine significantly reversed neuropathic pain behaviour dose- and time-dependently without motor impairment. Our data revealed that this effect was mediated by the α4β2 nAChRs by using competitive α4β2 antagonist dihydro-β-erythroidine. In addition, dFBr failed to potentiate the antiallodynic effect of morphine, which shows the effect of dFBr is unique to α4β2 nAChRs.
conclusionsThe present results suggest that allosteric modulation of α4β2 nAChR may provide new strategies in chronic neuropathic pain. SIGNIFICANCE: α4β2 nAChRs are involved in pain modulation. dFBr, a PAM at α4β2 nAChRs, potentiates the nicotine response dose-dependently in neuropathic pain. Thus, the present results suggest that allosteric modulation of α4β2* nAChR may provide new strategies in chronic neuropathic pain.
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