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Acta Physiologica Congress

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Acta Physiologica 2011; Volume 203, Supplement 686
Joint Congress of FEPS and Turkish Society of Physiological Sciences
9/3/2011-9/7/2011
Istanbul, Turkey


ARE MEMBRANE-BOUND G PROTEIN-COUPLED MELATONIN RECEPTORS MT1 AND MT2 REALLY NECESSARY FOR THE NEUROPROTECTIVE EFFECTS OF MELATONIN IN FOCAL CEREBRAL ISCHEMIA?
Abstract number: PC016

Kilic1 Ulkan, Yuksel2 Adnan, Yilmaz3 Bayram, Eyuboglu3 Signem, Ugur3 Milas, Kilic3 Ertugrul

1Bezmialem Vakif University, Faculty of Medicine, Department of Medical Biology, Istanbul, Turkey
2Bezmialem Vakif University, Faculty of Medicine, Department of Medical Genetic, Istanbul, Turkey
3Yeditepe University, Faculty of Medicine, Department of Physiology, Istanbul, Turkey

Objective: 

Melatonin is synthesized by the pineal gland in a circadian rhythm and predominantly acts through its MT1 and MT2 receptors. The roles of MT1 and MT2 in the neuroprotective effects of melatonin and cell signaling after cerebral ischemia were still unknown. In this study, we investigated the roles of MT1 and MT2 in the neuroprotective effects of melatonin in melatonin receptors 1-2 knockout mice.

Methods: 

Adult male melatonin receptors 1-2 knockout mice (mt1/2-/-), with a C3H/HeN strain background and their wt littermates were used. The animals were divided into four groups and submitted to 90 minutes of intraluminal middle cerebral artery (MCA) occlusion, followed by 24 hours of reperfusion and treated with melatonin (4 mg/ kg; i.p. day) or vehicle just after 90 min of ischemia. In these animals, infarct volume, edema formation, iNOS accumulation and signaling pathways, including CREB, ATF-1, p21, JNK1/2, p38 phosphorylation were analyzed.

Results:Here, we show that the infarct volume and brain edema do not differ between mt1/2-/- and WT animals but melatonin treatment decreases infarct volume in both groups and brain edema in WT animals after MCAo. Notably, melatonin's neuroprotective effect was even more pronounced in mt1/2-/- animals compared to WT animals. We also demonstrate that melatonin treatment decreases CREB, ATF-1 and p38 phosphorylation in both groups, while p21 and JNK1/2 were reduced only in melatonin-treated WT animals in the ischemic hemisphere. Furthermore, melatonin treatment decreased iNOS accumulation only in WT animals.

Conclusions: 

We provide evidence that neuroprotective efficacy of melatonin after ischemic injury in WT and MT1-2 knockout animals is independent from its membrane receptors.

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 203, Supplement 686 :PC016

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