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    Combined systemic administration of morphine and magnesium sulfate attenuates pain-related behavior in mononeuropathic rats
    (Elsevier Science Bv, 2002) Ulugol, A; Aslantas, A; Ipci, Y; Tuncer, A; Karadag, CH; Dokmeci, I
    The response to opioids is reduced in neuropathic pain states. We examined the effect of the combination of morphine (0.1 mg/kg) and magnesium sulfate (125 mg/kg) on behavioral signs of neuropathic pain in spinal nerve ligated rats. Administered alone, neither drug produced any effect, but the combination exerted a significant anti-allodynic effect, which was partially reversed by naloxone. These results suggest that combining low doses of magnesium sulfate with opiates might be an alternative in treating neuropathic pain, with reduced risk of side effects. (C) 2002 Elsevier Science B.V. All rights reserved.
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    Compound 48/80, a histamine-depleting agent, blocks the protective effect of morphine against electroconvulsive shock in mice
    (Assoc Bras Divulg Cientifica, 2000) Karadag, CH; Dokmeci, D; Dost, T; Ulugol, A; Dokmeci, I
    We have shown that morphine has an anticonvulsive effect against maximal electroconvulsive shock (MES) in mice, and this effect is antagonized by histamine Hi-receptor antagonists. Brain histamine is localized both in neurons and in mast cells, and morphine is known to enhance the turnover of neuronal histamine and to release histamine from mast cells. In the present experiments, compound 48/80 was injected chronically (0.5 mg/kg on day 1, 1 mg/kg on day 2, 2 mg/kg on day 3, 3 mg/kg on day 4, and 4 mg/kg on day 5, twice daily, ip) to deplete mast cell contents. Morphine (0.001-10 mg/kg, ip; N = 20) produced a dose-dependent anticonvulsive effect against MES seizure in mice with non-depleted mast cells, whereas it did not exert any anticonvulsive effect in mice with depleted mast cells. These results indicate that morphine produces its anticonvulsive effect against maximal electroconvulsive shock in mice by liberating histamine from mast cells.
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    Involvement of NMDA receptors and nitric oxide in the thermoregulatory effect of morphine in mice
    (Springer-Verlag Wien, 2000) Ulugol, A; Dost, T; Dokmeci, D; Akpolat, M; Karadag, CH; Dokmeci, I
    Morphine has long been known to have potent effects on body temperature. It has been suggested that both N-methl-D-aspartate (NMDA) receptors and nitric oxide (NO) pathway are involved in thermoregulation and also known to play important roles in some of morphine effects. The aim of this study was therefore to investigate the contribution of NMDA receptors and NO to the thermoregulatory effect of morphine. Morphine produced a hypothermic effect, especially at the dose of 10 mg/kg. Ketamine (5-40 mg/kg, i.p.) and N-G-nitro-L-arginine-methyl ester (L-Name, 1-100 mg/kg i.p.) also produced hypothermic effects with their higher doses. At doses which themselves produced no effect on colonic temperature in mice, both ketamine (10 mg/kg, i.p.) and L-NAME (10 mg/kg, i.p.) enhanced the hypothermic effect of morphine (10 mg/kg i.p.). These results further support the relationship between NO and NMDA receptors and suggest a possible role of NMDA-NO pathway in the thermoregulatory effect of morphine.
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    The role of histamine H-1-receptors in the anticonvulsive effect of morphine against maximal electroconvulsive shock in mice
    (Japanese Pharmacological Soc, 1996) Karadag, CH; Ulugol, A; Dokmeci, D; Dokmeci, I
    Morphine is known to release histamine from mast cells. It is also known that histamine receptors mediate some of morphine's effects on the central nervous system. The contribution of H-1- and H-2-receptors to the effect of morphine on maximal electroconvulsive shock in mice was investigated in the present experiments. Morphine showed a dose-dependent anticonvulsive effect, but produced spontaneous clonic convulsions at higher doses (100 mg/kg, i.p.). The anticonvulsive effect of morphine (1 mg/kg, i.p.) was antagonized by histamine Hi-receptor antagonists, dimethindene (0.1 mg/kg, i.p.), promethazine (0.4 mg/kg, i.p.) and pheniramine (30 mg/kg, i.p.), and naloxone (10 mg/kg, i.p.), but not by the H-2-receptor antagonist ranitidine (10-50 mu g, i.c.v.). These results show that morphine has an anticonvulsive effect via histamine H-1-receptors against maximal electroconvulsive shock in mice.