Neuronal Plasticity and Age-Related Functional Decline in the Motor Cortex

被引:4
|
作者
Inoue, Ritsuko [1 ]
Nishimune, Hiroshi [1 ,2 ]
机构
[1] Tokyo Metropolitan Inst Geriatr & Gerontol, Lab Neurobiol Aging, 35-2 Sakaecho,Itabashi Ku, Tokyo 1730015, Japan
[2] Tokyo Univ Agr & Technol, Dept Appl Biol Sci, 3-8-1 Harumicho, Fuchu, Tokyo 1838538, Japan
关键词
aging; CoQ(10); long-term potentiation; LTP; mitochondria; motor cortex; ubiquinone; LONG-TERM POTENTIATION; DIRECT-CURRENT STIMULATION; NONINVASIVE BRAIN-STIMULATION; BDNF VAL66MET POLYMORPHISM; LAYER-2/3 PYRAMIDAL CELLS; MESSENGER-RNA EXPRESSION; SYNAPTIC PLASTICITY; CORTICAL PLASTICITY; MITOCHONDRIAL BIOENERGETICS; INTRACORTICAL INHIBITION;
D O I
10.3390/cells12172142
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Physiological aging causes a decline of motor function due to impairment of motor cortex function, losses of motor neurons and neuromuscular junctions, sarcopenia, and frailty. There is increasing evidence suggesting that the changes in motor function start earlier in the middle-aged stage. The mechanism underlining the middle-aged decline in motor function seems to relate to the central nervous system rather than the peripheral neuromuscular system. The motor cortex is one of the responsible central nervous systems for coordinating and learning motor functions. The neuronal circuits in the motor cortex show plasticity in response to motor learning, including LTP. This motor cortex plasticity seems important for the intervention method mechanisms that revert the age-related decline of motor function. This review will focus on recent findings on the role of plasticity in the motor cortex for motor function and age-related changes. The review will also introduce our recent identification of an age-related decline of neuronal activity in the primary motor cortex of middle-aged mice using electrophysiological recordings of brain slices.
引用
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页数:17
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