Sutcu Recep, Yonden Zafer, Yilmaz Aysegul, Delibas Namik
Department of Biochemistry, School of Medicine, Suleyman Demirel University, Isparta, Turkey.
Mol Cell Biochem. 2006 Feb;283(1-2):101-5. doi: 10.1007/s11010-006-2385-4.
We investigated that the effects of melatonin on N-methyl-D: -aspartat receptor (NMDAR) subunits 2A and 2B concentrations and on markers of oxidative stress in hippocampus of rats treated with melatonin for 4 weeks. Animals were divided into four groups according to their melatonin doses (control group (C), n = 7; 5 mg/kg group (M5), n = 7; 10 mg/kg group (M10), n = 8; 20 mg/kg group (M20), n = 8) and received the melatonin as intraperitoneal injection. After 4 weeks of treatment, electrophoretic examination was done using sodium dodecyl sulfate/polyacrilamide gel electrophoresis (SDS-PAGE) and Western blotting in hippocampal homogenates of different groups. Malondialdehyde (MDA), an end product of lipid peroxidation, was assayed in all groups. There were significant increases in both NMDAR 2A; 5 mg/kg group (n = 3, p < 0.05), 10 mg/kg group (n = 3, p < 0.05), 20 mg/kg group (n = 3, p < 0.05) and NMDAR 2B expressions; 5 mg group (n = 3, p < 0.05), 10 mg group (n = 3, p < 0.05), 20 mg group (n = 3, p < 0.05), compared to the control group. No significant difference in MDA concentrations was found between groups. The present study clearly demonstrates that melatonin alters hippocampal NMDAR subunit concentrations in a dose-dependent manner without causing lipid peroxidation.
