Neuroprotective effect of melatonin against lipopolysaccharide-induced depressive-like behavior in mice

Accumulating evidence indicates an interaction between inflammation and depression since increased levels of pro-inflammatory cytokines are associated with depression-related symptoms. Melatonin is a hormone synthesized and secreted by the pineal gland with antioxidant, anti-inflammatory and antidep...

Full description

Saved in:

Bibliographic Details
Published in:	Physiology & behavior Vol. 188; pp. 270 - 275
Main Authors:	Taniguti, E.H., Ferreira, Y.S., Stupp, I.J.V., Fraga-Junior, E.B., Mendonça, C.B., Rossi, F.L., Ynoue, H.N., Doneda, D.L., Lopes, L., Lima, E., Buss, Z.S., Vandresen-Filho, S.
Format:	Journal Article
Language:	English
Published:	United States Elsevier Inc 01-05-2018
Subjects:	Brain-derived neurotrophic factor Depression Lipopolysaccharide Melatonin Oxidative stress Tumor necrosis factor-α Lipopolysaccharide Oxidative stress Depression Melatonin Brain-derived neurotrophic factor Tumor necrosis factor-α
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	Accumulating evidence indicates an interaction between inflammation and depression since increased levels of pro-inflammatory cytokines are associated with depression-related symptoms. Melatonin is a hormone synthesized and secreted by the pineal gland with antioxidant, anti-inflammatory and antidepressant-like effects. In this way, it would be interesting to evaluate the putative antidepressant-like effect of melatonin treatment in an acute inflammation mice model of depression. The present study aimed to investigate the effect of melatonin treatment on lipopolysaccharide (LPS) induced depressive-like behavior, neuroinflammation, oxidative stress and alteration on brain-derived neurotrophic fator (BDNF) levels. Mice were treated with melatonin (10 mg/kg, i.p.) 30 min before LPS (0.5 mg/kg, i.p.) injection. Twenty-four hours after LPS infusion, mice were submitted to the behavioral tests and, thereafter, biochemical determinations were performed. Melatonin treatment prevented LPS-induced depressive-like behavior in the forced swim and tail suspension tests with no alterations in locomotor activity evaluated in the open field test. Melatonin attenuated LPS-induced increase in tumor necrosis factor-α (TNF-α) and reduction of BDNF levels in the hippocampus. Treatment with melatonin also prevented LPS-induced increase in lipid peroxidation and the reduction of glutathione levels in the hippocampus. In conclusion, the present study suggests that melatonin treatment exerted neuroprotective effects against LPS-induced depressive-like behavior which may be related to reduction of TNF-α release, oxidative stress and modulation of BDNF expression. •Melatonin prevents lipopolysaccharide-induced depressive-like behavior.•Melatonin attenuates lipopolysaccharide-induced hippocampal expression of TNF-α.•Melatonin prevents increased oxidative stress induced by lipopolysaccharide.•Melatonin abolishes the reduction of BDNF levels induced by lipopolysaccharide.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0031-9384 1873-507X
DOI:	10.1016/j.physbeh.2018.02.034