Melatonin MT1 and MT2 receptor expression in Parkinson's disease

• Published in: Medical science monitor Vol. 16; no. 2; pp. BR61 - BR67
• Main Authors: Adi, Nikhil, Mash, Deborah C, Ali, Yousuf, Singer, Carlos, Shehadeh, Lina, Papapetropoulos, Spyridon
• Format: Journal Article
• Language: English
• Published: United States 01.02.2010
• Subjects: Aged; Aged, 80 and over; Amygdala - metabolism; Amygdala - pathology; Case-Control Studies; Cohort Studies; Down-Regulation; Female; Humans; Immunohistochemistry; Male; Parkinson Disease - genetics; Parkinson Disease - metabolism; Parkinson Disease - pathology; Receptor, Melatonin, MT1 - genetics; Receptor, Melatonin, MT1 - metabolism; Receptor, Melatonin, MT2 - genetics; Receptor, Melatonin, MT2 - metabolism; Reverse Transcriptase Polymerase Chain Reaction; Substantia Nigra - metabolism; Substantia Nigra - pathology
• ISSN: 1643-3750

Idiopathic Parkinson disease (PD) is a multi-system disorder with a multifactorial etiology and diverse clinical phenotype. Selective, regional dopaminergic neuronal degeneration in the substantia nigra and other CNS areas including the amygdala are observed in all patients. Apoptotic mechanisms resulting from oxidative stress and mitochondrial dysfunction have been implicated in the pathogenesis of the disease. Although the role of melatonin, a potent endogenous antioxidant, has been highlighted in PD there is no data on the expression of melatonin receptors in affected CNS regions. We conducted an RT-PCR-based study to determine the MT1 and MT2 receptors expression in whole brain post-mortem tissue from the amygdala and substantia nigra of well-characterized PD and control subjects. PD cases showed a statistically significant decrease of MT1 receptor expression in both substantia nigra (FC=5.11; p<0.05) and the amygdala (FC=3.11; p<0.001) versus normal controls. The expression of MT2 receptor expression was also decreased in both substantia nigra (FC=3.90; p<0.0001) and the amygdala (FC=1.91; p<0.001) versus normal controls. The results demonstrate a down-regulation of melatonin receptors in regions affected by PD, suggesting their possible involvement in the disease process. Future studies are needed to elucidate the role of melatonin and its receptors in the treatment/pathogenesis of PD.