Publication:
Melatonin pretreatment prevented the effect of dexamethasone negative alterations on behavior and hippocampal neurogenesis in the mouse brain

dc.contributor.authorNootchanart Rukseeen_US
dc.contributor.authorWalaiporn Tongjaroenbuangamen_US
dc.contributor.authorThanutchaporn Mahanamen_US
dc.contributor.authorPiyarat Govitrapongen_US
dc.contributor.otherMahidol University. National Institute for Child and Family Development
dc.contributor.otherMahidol University. Institute of Molecular Biosciences. Research Center for Neuroscience
dc.contributor.otherMahidol University. Center for Neuroscience and Department of Pharmacology
dc.date.accessioned2016-02-17T08:27:28Z
dc.date.accessioned2017-09-06T06:32:31Z
dc.date.available2016-02-17T08:27:28Z
dc.date.available2017-09-06T06:32:31Z
dc.date.created2016-02-17
dc.date.issued2014-02-28
dc.description.abstractGlucocorticoids 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.en_US
dc.identifier.citationMolecular Biology. Vol.143, (2014), 72-80en_US
dc.identifier.doi10.1016/j.jsbmb.2014.02.011
dc.identifier.urihttps://repository.li.mahidol.ac.th/handle/20.500.14594/7713
dc.language.isoengen_US
dc.rightsMahidol Universityen_US
dc.rights.holderElsevieren_US
dc.subjectMelatoninen_US
dc.subjectDepressionen_US
dc.subjectDexamethasoneen_US
dc.subjectStressen_US
dc.subjectNeurogenesisen_US
dc.subjectGlucocorticoid receptoren_US
dc.subjectERK1/2en_US
dc.subjectHippocampusen_US
dc.titleMelatonin pretreatment prevented the effect of dexamethasone negative alterations on behavior and hippocampal neurogenesis in the mouse brainen_US
dc.typeResearch Articleen_US
dspace.entity.typePublication
mods.location.urlhttp://www.sciencedirect.com/science/article/pii/S0960076014000405

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