Literature DB >> 23221868

Rufinamide attenuates mechanical allodynia in a model of neuropathic pain in the mouse and stabilizes voltage-gated sodium channel inactivated state.

Marc R Suter1, Guylène Kirschmann, Cedric J Laedermann, Hugues Abriel, Isabelle Decosterd.   

Abstract

BACKGROUND: Voltage-gated sodium channels dysregulation is important for hyperexcitability leading to pain persistence. Sodium channel blockers currently used to treat neuropathic pain are poorly tolerated. Getting new molecules to clinical use is laborious. We here propose a drug already marketed as anticonvulsant, rufinamide.
METHODS: We compared the behavioral effect of rufinamide to amitriptyline using the Spared Nerve Injury neuropathic pain model in mice. We compared the effect of rufinamide on sodium currents using in vitro patch clamp in cells expressing the voltage-gated sodium channel Nav1.7 isoform and on dissociated dorsal root ganglion neurons to amitriptyline and mexiletine.
RESULTS: In naive mice, amitriptyline (20 mg/kg) increased withdrawal threshold to mechanical stimulation from 1.3 (0.6-1.9) (median [95% CI]) to 2.3 g (2.2-2.5) and latency of withdrawal to heat stimulation from 13.1 (10.4-15.5) to 30.0 s (21.8-31.9), whereas rufinamide had no effect. Rufinamide and amitriptyline alleviated injury-induced mechanical allodynia for 4 h (maximal effect: 0.10 ± 0.03 g (mean ± SD) to 1.99 ± 0.26 g for rufinamide and 0.25 ± 0.22 g to 1.92 ± 0.85 g for amitriptyline). All drugs reduced peak current and stabilized the inactivated state of voltage-gated sodium channel Nav1.7, with similar effects in dorsal root ganglion neurons.
CONCLUSIONS: At doses alleviating neuropathic pain, amitriptyline showed alteration of behavioral response possibly related to either alteration of basal pain sensitivity or sedative effect or both. Side-effects and drug tolerance/compliance are major problems with drugs such as amitriptyline. Rufinamide seems to have a better tolerability profile and could be a new alternative to explore for the treatment of neuropathic pain.

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Year:  2013        PMID: 23221868     DOI: 10.1097/ALN.0b013e318278cade

Source DB:  PubMed          Journal:  Anesthesiology        ISSN: 0003-3022            Impact factor:   7.892


  9 in total

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2.  Discovery of Vixotrigine: A Novel Use-Dependent Sodium Channel Blocker for the Treatment of Trigeminal Neuralgia.

Authors:  David R Witty; Giuseppe Alvaro; Dominique Derjean; Gerard M P Giblin; Kevin Gunn; Charles Large; David T Macpherson; Valerie Morisset; Davina Owen; Joanne Palmer; Francois Rugiero; Simon Tate; Christopher A Hinckley; Himanshu Naik
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3.  Blockade of Nav1.8 currents in nociceptive trigeminal neurons contributes to anti-trigeminovascular nociceptive effect of amitriptyline.

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Journal:  Neuromolecular Med       Date:  2013-11-30       Impact factor: 3.843

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5.  Carbamazepine potentiates the effectiveness of morphine in a rodent model of neuropathic pain.

Authors:  Michael R Due; Xiao-Fang Yang; Yohance M Allette; Aaron L Randolph; Matthew S Ripsch; Sarah M Wilson; Erik T Dustrude; Rajesh Khanna; Fletcher A White
Journal:  PLoS One       Date:  2014-09-15       Impact factor: 3.240

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Authors:  Harpreet S Sidhu; Akshay Sadhotra
Journal:  Front Pharmacol       Date:  2016-08-25       Impact factor: 5.810

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Journal:  Nature       Date:  2016-06-06       Impact factor: 49.962

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Review 9.  Spider Knottin Pharmacology at Voltage-Gated Sodium Channels and Their Potential to Modulate Pain Pathways.

Authors:  Yashad Dongol; Fernanda Caldas Cardoso; Richard J Lewis
Journal:  Toxins (Basel)       Date:  2019-10-29       Impact factor: 4.546

  9 in total

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