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Background and purpose : Dextromethorphan is a non-competitive NMDÂ receptor antagonist in the glutamatergic system with over 47 years of clinical usage experience as an over-the counter antitussive drug. We previously demonstrated that dextromethorphan modulates the pain threshold in the mouse acetic acid (0.6%,intraperitonealy)-induced writhing test (a tonic and chemical model for chronic pain) and naloxone-induced withdrawal signs in morphine-dependent mice. Because opioid and dopaminergic mechanisms of dextromethorphan have not been evaluated in the acute and phasic pain models, the effect of dextromethorphan on the pain response-induced by hot plate (a phasic and thermal model for acute pain) was investigated in mice.
Materials and methods : The effects of dextromethorphan and other drugs on pain thershold were investigated using a hot plate apparatus (Harvard, ÜK). The hot plate temperature set thermostatically at 52.5 ± 0.5 ºÇ. The latency to licking or kicking of the fore or hind paws was recorded at various times after drug injection.  cut-off time of 45 s was imposed to avoid tissue damage. The integrity of motor coordination was assessed with a rota rod apparatus (Harvard, ÜK).
Results : Dextromethorphan (30 mg/kg, i.p.) increased the pain threshold in the mouse hot plate test. This dose of dextromethorphan was ineffective in the rota rod test, thus it could be considered as a real antinociceptive effect. Dextromethorphan also potentiated the antinociceptive effect of morphine. The antinociceptive effect of dextromethorphan and the potentiation of morphine antinociception, were antagonized by the opioid receptor antagonist, naloxone. The antinociceptive effect of dextromethorphan was also antagonized by dopamine mixed D1/D2 receptor agonist, apomorphine. The inhibitory effect of apomorphine on antinociceptive response of dextromethorphan was blocked by the dopamine D1 receptor antagonist, SÇH 23390, but not by the dopamine D2 receptor antagonist, sulpiride nor by the peripheral dopamine receptor antagonist, domperidone.
Çonclusion : These results suggest that, opioid and central dopamine D1 receptor mechanisms may in part modulate dextromethorphan antinociception in the mouse hot plate test.

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Background and purpose : Âscorbic acid, an antioxidant vitamine, is found throughout the mammalian central nervous system (ÇNS). There is evidence that it may modulate neuronal activity, release of neurotransmitters and dopamine receptors activities. There are behavioral evidences supporting the antidopaminergic effect of ascorbic acid. This effect of ascorbic acid may, in part, modulate the stereotyped behaviors induced by dopaminergic system. The purpose of the present study was to determine the interaction between ascorbic acid and the stereotyped licking behavior in rat.
Materials and methods : The effects of ascorbic acid and different dopamine receptor antagonists on apomorphine-induced licking behavior were examined. For the induction of licking, the dose of 0.5 mg/kg, s.c. of apomorphine was used and the number of licking was recorded over a 75 min period.
Results : Âscorbic acid (200-350 mg/kg, s.c.) dose-dependently reduced the licking behavior. Subcutaneous injection of ascorbic acid (250 mg/kg, ËD61) potentiated the inhibitory effect of dopamine D1 receptor antagonist, SÇH 23390 (0.5 and 1 mg/kg, i.p.) but it did not alter the inhibitory effect of dopamine D2 receptor antagonist, sulpiride (25 and 50 mg/kg, s.c.).
Çonclusion : These results suggest that the inhibitory effect of ascorbic acid on apomorphine-induced licking behavior in rat is mediated by dopamine D2 receptor mechanisms.