Neuropathic Pain Can Be Relieved by Drugs That Are Use-dependent Sodium Channel Blockers

Tanelian, Darrell L.; Brose, William G.

doi:10.1097/00000542-199105000-00026

Cited by 188 publications

(73 citation statements)

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“…In humans, neuropathic pain can be relieved by use-dependent sodium channel blockers, carbamazepine and mexiletine (Tanelian and Brose 1991). Intravenous administration of mexiletine (3-15 mg/kg) or the local anesthetic lidocaine (5-25 mg/kg) have been shown to decrease the sensitivity of spontaneously active fibers in rat sciatic neuromas to mechanical stimulation (Chabal et al 1989).…”

Section: Mechanism Of U50488 Induced Suppression Of Pelvic Nerve Actmentioning

confidence: 99%

Sodium Channel Blocking Actions of the κ-Opioid Receptor Agonist U50,488 Contribute to Its Visceral Antinociceptive Effects

Joshi

Kardos

et al. 2002

Journal of Neurophysiology

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. Sodium channel blocking actions of the -opioid receptor agonist U50,488 contribute to its visceral antinociceptive effects. J Neurophysiol 87: 1271-1279, 2002; 10.1152/jn.00624.2001. The goal of the present study was to determine whether the -opioid receptor agonist (ORA) U50,488 attenuates behavioral and primary afferent nerve responses to noxious colorectal distension (CRD) by sodium channel blockade. We tested the analgesic -ORA (Ϯ)-trans U50,488, its enantiomers (Ϫ)-trans (1S,2S)-U50,488 and non -ORA (ϩ)-trans (1R,2R)-U50,488, and/or its diastereomer (Ϫ)-cis (1S,2R)-U50,488 for their ability to attenuate visceromotor and pelvic nerve afferent fiber responses to noxious CRD in vivo and voltage-activated sodium current in colon sensory neurons in vitro. In unanesthetized rats, subcutaneous administration of U50,488, (1S,2S)-U50,488, and (1R,2R)-U50,488 attenuated the behavioral visceromotor response to noxious CRD; the rank order of potency was: (1S,2S)-U50,488 Ͼ U50,488 Ͼ Ͼ (1R,2R)-U50,488. U50,488 and its stereoisomers also inhibited responses of decentralized pelvic nerve afferent fibers to noxious CRD in a dose-dependent manner. Cumulative doses of 16 mg/kg of (1S,2S)-U50,488, (1S,2R)-U50,488, and (1R,2R)-U50,488 reduced responses to a mean 29, 30, and 47% of control, respectively. The mean inhibitory doses of these drugs were not different (range: 6.6 -10.8 mg/kg). Sodium channel blockers mexiletine and carbamazepine mimicked the effect of U50,488. In contrast, the -ORAs dynorphin (1-13) and ICI 204,488 were ineffective in attenuating pelvic nerve activity. Perfusion of (1S,2S)-U50,488, (1S,2R)-U50,488, or (1R,2R)-U50,488 on colon sensory neurons in vitro decreased voltage-activated sodium currents. This inhibition by U50,488 and its stereoisomers was not opioid receptor-mediated because it could not be reversed by the opioid receptor antagonist naloxone and was also not a G protein-mediated effect. The results reported here suggest that the visceral antinociceptive effects of U50,488 and its stereoisomers are contributed to by their peripheral sodium channel blocking actions. I N T R O D U C T I O NThe mechanisms and modulation of visceral pain have been extensively examined using colorectal distension (CRD) as a noxious visceral stimulus. Previous studies employing CRD have documented the ability of -opioid receptor agonists (ORAs) like U50,488 to attenuate pseudaffective visceromotor and cardiovascular responses to noxious CRD following their systemic, but not intrathecal administration (Danzebrink et al. 1995; Harada et al. 1995a,b). A peripheral, visceral antinociceptive action of U50,488 has been demonstrated. U50,488 was shown to dose dependently inhibit responses of mechanosensitive pelvic nerve afferent fibers to noxious colorectal or urinary bladder distension in the rat Su et al. 1997a,b). This inhibition could not be completely antagonized by very high doses of naloxone or by two -opioid receptor-selective antagonists, nor-Binaltorphimine dihydrochloride (nor-BNI) and DIPPA. Furthermore, ...

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Section: Mechanism Of U50488 Induced Suppression Of Pelvic Nerve Actmentioning

confidence: 99%

Sodium Channel Blocking Actions of the κ-Opioid Receptor Agonist U50,488 Contribute to Its Visceral Antinociceptive Effects

Joshi

Kardos

et al. 2002

Journal of Neurophysiology

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“…Lidocaine and mexiletine are known to be useful drugs whose antinociceptive activities are increased in diabetes (5). Pain related to diabetic neuropathy is difficult to control by nonsteroidal anti-inflammatory drugs (7).…”

Section: *Corresponding Author Fax: +81-86-235-6664mentioning

confidence: 99%

“…Diabetic neuropathy can be associated with a sensation of burning or tactile hypersensitivity (4). Since pain related to diabetic neuropathy is difficult to control by nonsteroidal anti-inflammatory drugs, such pain is treated with lidocaine and mexiletine (5).…”

mentioning

confidence: 99%

Antinociceptive Effect of Vitamin K2 (Menatetrenone) in Diabetic Mice

Onodera

Zushida

Kamei

2001

Japanese Journal of Pharmacology

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ABSTRACT-The antinociceptive effect of vitamin K2 (menatetrenone) in diabetic mice was examined using a tail-pressure test. Intraperitoneal injection of menatetrenone (10 -100 mg/ kg) produced a dosedependent increase in the nociceptive threshold in diabetic mice. There was no significant difference between non-diabetic and diabetic mice in the menatetrenone-induced changes in the nociceptive threshold. The results suggest the therapeutical usefulness of menatetrenone for treating painful diabetic neuropathy and osteoporosis.

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“…This therapeutic effect is due to dose dependent sodium channels block [7,8] both peripherally and centrally [9].…”

Section: Introductionmentioning

confidence: 99%

Comparative Study between Intravenous Ketamine and Lidocaine Infusion in Controlling of Refractory Trigeminal Neuralgia

Mogahed¹,

Anwar²,

Mohamed³

2017

J Anesth Clin Res

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Neuropathic Pain Can Be Relieved by Drugs That Are Use-dependent Sodium Channel Blockers

Cited by 188 publications

References 0 publications

Sodium Channel Blocking Actions of the κ-Opioid Receptor Agonist U50,488 Contribute to Its Visceral Antinociceptive Effects

Sodium Channel Blocking Actions of the κ-Opioid Receptor Agonist U50,488 Contribute to Its Visceral Antinociceptive Effects

Antinociceptive Effect of Vitamin K2 (Menatetrenone) in Diabetic Mice

Comparative Study between Intravenous Ketamine and Lidocaine Infusion in Controlling of Refractory Trigeminal Neuralgia

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