Mazindol and lidocaine are antinociceptives in the mouse formalin model: involvement of dopamine receptor

Bittencourt, Alvorita Leite; Takahashi, Reinaldo Ν.

doi:10.1016/s0014-2999(97)00182-9

Cited by 32 publications

(13 citation statements)

References 21 publications

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“…In the present study, carbamazepine and lidocaine as sodium channel blockers induced dose-dependently antinociception, which is supported by the other works (Kiguchi et al, 2004;Shannon et al, 2005;Mashimoto et al, 1998;Bittencourt & Takahashi, 1997;Hao et al, 1999Hao et al, , 2001. As well as of transmission of pain, the function of sodium channels is exaggerated and/or Int J Neurosci Downloaded from informahealthcare.com by University of Auckland on 12/07/14…”

Section: Discussionsupporting

confidence: 89%

On the Mechanism of Carbamazepin-Induced Antinociception in the Formalin Test

Sahebgharani

Hossein-Abad

Zarrindast

2006

International Journal of Neuroscience

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In the present study, the effect of lidocaine (a sodium channel blocker) on carbamazepine-induced antinociception, in formalin test was investigated. Intraperitoneal (i.p.) administration of different doses of carbamazepine (3.5, 7, 15, and 30 mg/kg) induced a dose-dependent antinociception in mice, in the first and second phases of the test. Different doses of lidocaine as a sodium channel blocker (5, 10, and 20 mg/kg, i.p.) also induced antinociception in both phases of the formalin test. It is noted that lidocaine could potentiate the response of carbamazepine in the first, but not in the second, phase of the formalin test. Meanwhile i.p. administration of different doses of Prazosin, alpha1 adrenoceptor antagonist (0.125, 0.25, and 0.5 mg/kg), Yohimbine, alpha2 adrenoceptor antagonist (0.25, 0.5, and 1 mg/kg), Bicuculline, GABAA receptor antagonist (1.5 and 3 mg/kg), and CGP 35348, GABAB receptor antagonist (100 and 200 mg/kg) exert dose-dependent antinociceptive effect in both phases of the formalin test. It should be noted that bicuculline 0.75 mg/kg by itself increased pain score in the second phase of the formalin test, indicating that blockade of GABAA receptor subtype may induce chronic pain. None of the aforementioned drugs could alter the antinociceptive response of carbamazepine in the formalin test. It is concluded that sodium channel mechanisms may be involved partly in the antinociceptive induced by carbamazepine.

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Section: Discussionsupporting

confidence: 89%

On the Mechanism of Carbamazepin-Induced Antinociception in the Formalin Test

Sahebgharani

Hossein-Abad

Zarrindast

2006

International Journal of Neuroscience

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“…In some previous reports, pretreatment with lidocaine (10–30 mg/kg, i.p.) antagonized the behavioral response in both phases of the test in mice (e.g., Bittencourt and Takahashi, 1997; Sahebgharani et al, 2006). However, Hitosugi et al (1999) found that pretreating mice with the same doses of lidocaine (i.p.)…”

Section: Discussionmentioning

confidence: 97%

Inhibitory effect of lidocaine on pain and itch using formalin-induced nociception and 5′-guanidinonaltrindole-induced scratching models in mice: Behavioral and neuroanatomical evidence

Inan

Dun

Cowan

2009

European Journal of Pharmacology

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The aim of this study was to establish the effect of lidocaine, a local anesthetic, on pain and itch using formalin-induced nociception and kappa opioid antagonist-induced scratching models in mice. We investigated if local intradermal pretreatment (at −10 min) with lidocaine N-ethyl bromide (lidocaine, 2%, 0.1 ml) antagonizes behavioral responses and prevents c-fos expression induced by pain and itch. Male, Swiss Webster mice (25-30 g, n=6-10) were used. Formalin (5%, 20 µl, s.c.) or saline was administered to the right dorsal hindpaw and the time spent licking this paw was recorded at 0-10 min and 20-35 min. For itching, mice were challenged with 5′-guanidinonaltrindole (GNTI, 0.3 mg/kg, s.c., behind the neck) or saline and the number of neck-directed scratches with hindpaws was counted for 30 min. C-fos immunohistochemistry was performed in lumbar (for pain) and cervical (for scratching) spinal sections 2 h after respective treatments. We found that lidocaine (a) antagonizes both formalin-induced pain and GNTI-induced scratching and (b) prevents c-fos expression evoked by pain (medial side of the superficial layer and deeper layers of the dorsal horn) and itch (lateral side of the superficial layer of the dorsal horn). Additionally, GNTI caused c-fos activation in mice wearing an Elizabethan collar (to prevent scratching of the neck) suggesting that GNTI provokes c-fos expression by inducing an itch sensation. Our results highlight the antipruritic properties of lidocaine and argue for its comprehensive clinical testing against pruritic states.

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“…35,36) This result suggests that (Ϫ)-carvone might also produce antinociceptive effects by voltage-gated Na ϩ channel blockade.…”

Section: )mentioning

confidence: 90%

Antinociceptive Activity of (-)-Carvone: Evidence of Association with Decreased Peripheral Nerve Excitability

Gonçalves

Oliveira

Benedito

et al. 2008

Biological & Pharmaceutical Bulletin

111

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(؊)-Carvone is a monoterpene ketone that is the main active component of Mentha plant species like Mentha spicata. This study aimed to investigate the antinociceptive activity of (؊)-carvone using different experimental models of pain and to investigate whether such effects might be involved in the nervous excitability elicited by others monoterpenes. In the acetic acid-induced writhing test, we observed that (؊)-carvone-treated mice exhibited a significant decrease in the number of writhes when 100 and 200 mg/kg was administered. It was also demonstrated that (؊)-carvone inhibited the licking response of the injected paw when 100 and 200 mg/kg was administered (i.p.) to mice in the first and second phases of the formalin test. Since naloxone (5 mg/kg, s.c.), an opioid antagonist, showed no influence on the antinociceptive action of (؊)-carvone (100 mg/kg), this suggested nonparticipation of the opioid system in the modulation of pain induced by (؊)-carvone. Such results were unlikely to be provoked by motor abnormality, since (؊)-carvone-treated mice did not exhibit any performance alteration on the Rota-rod apparatus. Because the antinociceptive effects could be associated with neuronal excitability inhibition, we performed the single sucrose gap technique and observed that (؊)-carvone (10 mM) was able to reduce the excitability of the isolated sciatic nerve through a diminution of the compound action potential amplitude by about 50% from control recordings. We conclude that (؊)-carvone has antinociceptive activity associated with decreased peripheral nerve excitability.

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Mazindol and lidocaine are antinociceptives in the mouse formalin model: involvement of dopamine receptor

Cited by 32 publications

References 21 publications

On the Mechanism of Carbamazepin-Induced Antinociception in the Formalin Test

On the Mechanism of Carbamazepin-Induced Antinociception in the Formalin Test

Inhibitory effect of lidocaine on pain and itch using formalin-induced nociception and 5′-guanidinonaltrindole-induced scratching models in mice: Behavioral and neuroanatomical evidence

Antinociceptive Activity of (-)-Carvone: Evidence of Association with Decreased Peripheral Nerve Excitability

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