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Öğe Antihyperalgesic, but not antiallodynic, effect of melatonin in nerve-injured neuropathic mice: Possible involvements of the L-arginine-NO pathway and opioid system(Pergamon-Elsevier Science Ltd, 2006) Ulugol, A; Dokmeci, D; Guray, G; Sapolyo, N; Ozyigit, F; Tamer, MThe present study was undertaken to determine the effects of intracerebroventricular (i.c.v.) and intraperitoneal (i.p.) melatonin on mechanical allodynia and thermal hyperalgesia in mice with partial tight ligation of the sciatic nerve, and how the nitric oxide (NO) precursor L-arginine and the opiate antagonist naloxone influence this effect. A plantar analgesic meter was used to assess thermal hyperalgesia, and nerve injury-induced mechanical hyperalgesia was assessed with von Frey filaments. 1-5 weeks following the surgery, marked mechanical allodynia and thermal hyperalgesia developed in neuropathic mice. Intracerebroventricular and intraperitoneal melatonin, with its higher doses, produced a blockade of thermal hyperalgesia, but not mechanical allodynia. Administration of both L-arginine and naloxone, at doses which produced no effect on their own, partially reversed antihyperalgesic effect of melatonin. These results suggest that although it has different effects on neuropathic pain-related behaviors, melatonin may have clinical utility in neuropathic pain therapy in the future. It is also concluded that L-arginine-NO pathway and opioidergic system are involved in the antihyperalgesic effect of melatonin in nerve-injured mice. (c) 2005 Elsevier Inc. All rights reserved.Öğe 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, IWe 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.Öğe 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, IMorphine 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.Öğe L-carnitine inhibits ethanol-induced gastric mucosal injury in rats(Springer Heidelberg, 2005) Dokmeci, D; Akpolat, M; Aydogdu, N; Doganay, L; Turan, FNL-carnitine is a quaternary amine that is essential for the normal oxidation of long-chain fatty acids by mitochondria. It is known that L-carnitine and its derivatives prevent the formation of reactive oxygen species, scavenge free radicals and protect cells from peroxidative stress. Oxygen-derived free radicals and lipid peroxidation products play a critical role in the pathogenesis of ethanol-induced gastric mucosal injury. The aim of the present study was to determine the effect of L-camitine on lipid peroxidation induced by ethanol in the rat stomach. In our study, gastric mucosal injury was induced by the intragastric administration of 1 ml of absolute ethanol. Test compounds were given to rats by gavage 30 min before the ethanol administration. The animals were killed 60 min after the administration of ethanol. The stomach of each animal was removed. Mucosal damage was evaluated by macroscopic examination, histological analysis and by measurement of lipid peroxidation and glutathione activity. The intragastric administration of ethanol induced hyperemia and hemorrhagic erosions in the rat stomachs. L-camitine significantly prevented gastric ulcerogenesis induced by ethanol and decreased the ulcer index. Plasma and gastric lipid peroxidation that was increased significantly by ethanol was decreased after treatment with L-camitine. Ethanol treatment decreased significantly the gastric glutathione levels, and pretreatment with L-camitine increased them significantly. Based on these data, the beneficial effects of L-camitine on ethanol-induced gastric mucosal injury may be attributed to its antiperoxidative effects.Öğe The role of histamine H-1 receptors in the thermoregulatory effect of morphine in mice(Elsevier Science Bv, 1996) Ulugol, A; Karadag, HC; Dokmeci, D; Baldik, Y; Dokmeci, IMorphine is known to release histamine from mast cells and increase the turnover of neuronal histamine. It is also known that histamine receptors mediate some of the morphine effects. The contribution of histamine H-1 and H-2 receptors to the thermoregulatory effect of morphine in mice was investigated in the present experiments. Morphine produced a hypothermic effect, especially at the dose of 10 mg/kg. Although the histamine H-1 receptor antagonist, dimethindene (0.1 mg/kg, i.p.), attenuated the hypothermic effect of morphine (10 mg/kg), a histamine H-2 receptor antagonist, ranitidine (100 mg/kg, i.p.), had no effect. These results suggest that the hypothermic effect of morphine in mice is mediated, at least partly, through histamine H-1 receptors.Öğe 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, IMorphine 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.Öğe The role of nitric oxide in the protective effect of insulin against pentylenetetrazole-induced seizures in mice(John Wiley & Sons Ltd, 2000) Ulugol, A; Arikan, E; Dost, T; Dokmeci, D; Karadag, HC; Dokmeci, IBoth insulin, depending on the glycemic state, and nitric oxide (NO), depending on the experimental conditions, have been suggested to have either proconvulsant or anticonvulsant effects. It is also known that NO plays an important role in some of the peripheral effects of insulin. The aim of the present study was to investigate the effects of NO and insulin against convulsions produced by pentylenetetrazole (PTZ, 60 mg/kg, i.p.) in mice and whether NO plays a role in the effect of insulin. Nitric oxide synthase (NOS) inhibitor, N-G-nitro-L-arginine-methyl ester (L-NAME, 1-100 mg/kg, i.p.) shortened the onset of PTZ-induced convulsions and increased the incidence and mortality rate, at the higher doses. Insulin (1 U/kg, i.p.), when given with dextrose (3 g/kg, i.p.) to counteract the hypoglycemic effect of the hormone, prolonged the onset of convulsions and decreased the incidence and mortality rate. L-NAME pretreatment (3 mg/kg, i.p.), at the dose which it produced no effect on PTZ-induced convulsions, attenuated the protective effect of 1 U/kg insulin + 3 g/kg dextrose combination significantly. Concomitant administration of the NO synthesis precursor, L-arginine (500 mg/kg), completely reversed this facilitatory effect of L-NAME. Our results indicate that NO has a protective effect against PTZ-induced convulsions in mice; insulin has a similar effect when given with dextrose; and, NO production may play an important role in the anticonvulsant effect of insulin.Öğe The role of nitric oxide in the protective effect of insulin against pentylenetetrazole-induced seizures in mice [Meeting Abstract](Springer-Verlag, 2000) Ulugol, A; Arikan, E; Dost, T; Dokmeci, D; Karadag, H; Dokmeci, I[Abstract Not Available]
