| Literature DB >> 27379735 |
Zhiqiang Xu1,2, Xiaobo Guo2, Yong Yang3, Donovan Tucker4, Yujiao Lu4, Ning Xin1, Gaocai Zhang1,2, Lingli Yang1, Jizhen Li5, Xiangdong Du3, Quanguang Zhang6, Xingshun Xu7,8.
Abstract
Major depressive disorder (MDD) is one of the leading forms of psychiatric disorders, characterized by aversion to mobility, neurotransmitter deficiency, and energy metabolic decline. Low-level laser therapy (LLLT) has been investigated in a variety of neurodegenerative disorders associated with mitochondrial dysfunction and functional impairments. The goal of this study was to examine the effect of LLLT on depression-like behaviors and to explore the potential mechanism by detecting mitochondrial function following LLLT. Depression models in space restriction mice and Abelson helper integration site-1 (Ahi1) knockout (KO) mice were employed in this work. Our results revealed that LLLT effectively improved depression-like behaviors, in the two depression mice models, by decreasing immobility duration in behavioral despair tests. In addition, ATP biosynthesis and the level of mitochondrial complex IV expression and activity were significantly elevated in prefrontal cortex (PFC) following LLLT. Intriguingly, LLLT has no effects on ATP content and mitochondrial complex I-IV levels in other tested brain regions, hippocampus and hypothalamus. As a whole, these findings shed light on a novel strategy of transcranial LLLT on depression improvement by ameliorating neurotransmitter abnormalities and promoting mitochondrial function in PFC. The present work provides concrete groundwork for further investigation of LLLT for depression treatment.Entities:
Keywords: Depression; Low-level laser therapy; Mitochondria; Neurotransmitter deficiency
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Year: 2016 PMID: 27379735 PMCID: PMC5215986 DOI: 10.1007/s12035-016-9983-2
Source DB: PubMed Journal: Mol Neurobiol ISSN: 0893-7648 Impact factor: 5.590