Investigation of the Effects of MK-801 on Oxidative Stress, Inflammation and Ghrelin Levels in Brain Tissue in Convulsions Caused by Scopolamine Administration and Feeding in Starving Mice

Abstract

In this study, the effect of MK-801, one of the noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists, on convulsions that occurred in mice that were given scopolamine and then fed experimentally after 48 hours of fasting was investigated. In our study, 36 Balb/C adult male mice weighing 25-30 g were used. Mice were randomly selected and divided into 6 groups. These are control, scopolamine (3 mg/kg/i.p.), low dose MK-801 (0.17 mg/kg/i.p.), high dose MK-801 (0.51 mg/kg/i.p.), scopolamine + low dose MK- 801 and scopolamine+ high dose MK-801 groups. After the injections, the animals in all groups were taken to the monitoring cages and fed 20 minutes after the injections. Convulsion onset times and severity of animals in all groups were measured. At the end of the follow-up period, animals in all groups, including the control group, were sacrificed under anesthesia with ketamine (50 g/kg/i.p.) and xylazine (10 mg/kg/i.p.), their blood was drawn and brain tissues were isolated. Blood ghrelin levels of all animals and some oxidative stress and inflammation markers and ghrelin levels in brain tissue were measured. Analysis of the study was done using SPSS v16.0 statistical program. The statistical significance level was taken as p<0.05 in the calculations. It was observed that scopolamine administration caused a decrease in catalase and superoxide dismutase activities and ghrelin levels, and increased protein oxidation and inflammatory response. MK-801 treatment has been found to both delay the incidence of convulsions and suppress oxidative stress and inflammation (p<0.05). We think that these effects of MK-801 are due to the increased ghrelin level, as the application of MK-801 also causes an increase in the level of ghrelin.

Keywords: Convulsion, Scopolamine, MK-801, Oxidative Stress, Ghrelin

DOI: 10.7176/JSTR/7-10-01