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KMID : 0892920170260020104
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Experimental Neurobiology
2017 Volume.26 No. 2 p.104 ~ p.112
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A High-fat Diet Induces a Loss of Midbrain Dopaminergic Neuronal Function That Underlies Motor Abnormalities
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Jang Yun-Seon
Lee Min-Joung
Han Jeong-Su
Kim Soo-Jeong
Ryu Il-Hwan
Ju Xianshu
Ryu Min-Jeong
Chung Woo-Suk
Oh Eung-Seok
Kweon Gi-Ryang
Heo Jun-Young
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Abstract
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Movement defects in obesity are associated with peripheral muscle defects, arthritis, and dysfunction of motor control by the brain. Although movement functionality is negatively correlated with obesity, the brain regions and downstream signaling pathways associated with movement defects in obesity are unclear. A dopaminergic neuronal pathway from the substantia nigra (SN) to the striatum is responsible for regulating grip strength and motor initiation through tyrosine hydroxylase (TH) activity-dependent dopamine release. We found that mice fed a high-fat diet exhibited decreased movement in open-field tests and an increase in missteps in a vertical grid test compared with normally fed mice. This motor abnormality was associated with a significant reduction of TH in the SN and striatum. We further found that phosphorylation of c-Jun N-terminal kinase (JNK), which modulates TH expression in the SN and striatum, was decreased under excess-energy conditions. Our findings suggest that high calorie intake impairs motor function through JNK-dependent dysregulation of TH in the SN and striatum.
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KEYWORD
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Dopaminergic neuron, Obesity, Motor abnormality, Tyrosine hydroxylase
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