Simple jQuery Dropdowns
Please use this identifier to cite or link to this item:
Title: Melatonin pretreatment prevented the effect of dexamethasone negative alterations on behavior and hippocampal neurogenesis in the mouse brain
Authors: Nootchanart Ruksee
Walaiporn Tongjaroenbuangam
Thanutchaporn Mahanam
Piyarat Govitrapong
Mahidol University. National Institute for Child and Family Development
Mahidol University. Institute of Molecular Biosciences. Research Center for Neuroscience
Mahidol University. Center for Neuroscience and Department of Pharmacology
Keywords: Melatonin;Depression;Dexamethasone;Stress;Neurogenesis;Glucocorticoid receptor;ERK1/2;Hippocampus
Issue Date: 28-Feb-2014
Citation: Molecular Biology. Vol.143, (2014), 72-80
Abstract: Glucocorticoids play various physiological functions via the glucocorticoid receptor (GR). Glucocorticoid is associated with the pathophysiology of depression. Dexamethasone (DEX), a synthetic GR agonist, has a greater affinity for GR than the mineralocorticoid receptor (MR) in the hippocampus of pigs and may mimic the effects of GR possession. DEX decreases neurogenesis and induces damage to hippocampal neurons that is associated with depressive-like behavior. Melatonin, a hormone mainly synthesized in the pineal gland, is a potent free radical scavenger and antioxidant. Melatonin alters noradrenergic transmission in depressed patients. It may be interesting to further explore the mechanism of melatonin that is associated with the role of stress as a key factor to precipitate depression and as a factor altering neurogenesis. In this study, we assessed the capability of melatonin to protect the hippocampus of mouse brains to counteract the effects of chronic DEX treatment for 21 days on depressive-like behavior and neurogenesis. Our results revealed that chronic administration of DEX induced depressivelike behavior and that this could be reversed by pretreatment with melatonin. Moreover, the number of 5-bromo-2-deoxyuridine (BrdU)-immunopositive cells and doublecortin (DCX; the neuronal-specific marker) protein levels were significantly reduced in the DEX-treated mice. Pretreatment with melatonin was found to renew BrdU and DCX expression in the dentate gyrus. Furthermore, pretreatment withmelatonin prevented DEX-induced reductions in GR and an extracellular-signal-regulated kinase (ERK1/2) in the hippocampal area. Melatonin may protect hippocampal neurons from damage and reverse neurogenesis after chronic DEX by activating brain-derived neurotrophic (BDNF) and ERK1/2 cascades. These results revealed that melatonin pretreatment prevented the reduction of cell proliferation, immature neuron precursor cells, and GR and ERK1/2 expression. This finding indicates that melatonin attenuates the DEX-induced depressive-like behavior, supporting the notion that melatonin possesses anti-stress and neurogenic actions.
Appears in Collections:MB-Article

Files in This Item:
File Description SizeFormat 
cf-ar-nootchan-2014.pdf3.82 MBAdobe PDFView/Open

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.