TY - JOUR
T1 - Low-Level Laser Irradiation Improves Depression-Like Behaviors in Mice
AU - Xu, Zhiqiang
AU - Guo, Xiaobo
AU - Yang, Yong
AU - Tucker, Donovan
AU - Lu, Yujiao
AU - Xin, Ning
AU - Zhang, Gaocai
AU - Yang, Lingli
AU - Li, Jizhen
AU - Du, Xiangdong
AU - Zhang, Quanguang
AU - Xu, Xingshun
N1 - Funding Information:
This study was supported by the grants from National Natural Science Foundation of China (81071095, 81120108011, and 81200893); Jiangsu Province Science and Technology Project (BK20151197), Suzhou Science and Technology Project (SYS201372 and LCZX201316); the Priority Academic Program Development of Jiangsu Higher Education Institutions of China; and a Research Grant NS086929 from the National Institute of Neurological Disorders and Stroke, National Institutes of Health, USA. The funders have no role in study design and data collection.
Publisher Copyright:
© 2016, Springer Science+Business Media New York.
PY - 2017/8/1
Y1 - 2017/8/1
N2 - 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.
AB - 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.
KW - Depression
KW - Low-level laser therapy
KW - Mitochondria
KW - Neurotransmitter deficiency
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U2 - 10.1007/s12035-016-9983-2
DO - 10.1007/s12035-016-9983-2
M3 - Article
C2 - 27379735
AN - SCOPUS:84977070688
SN - 0893-7648
VL - 54
SP - 4551
EP - 4559
JO - Molecular Neurobiology
JF - Molecular Neurobiology
IS - 6
ER -