A combined TMS-EEG study of short-latency afferent inhibition in the motor and dorsolateral prefrontal cortex

被引:30
|
作者
Noda, Yoshihiro [1 ,3 ]
Cash, Robin F. H. [1 ,4 ]
Zomorrodi, Reza [1 ]
Dominguez, Luis Garcia [1 ]
Farzan, Faranak [1 ,2 ,3 ]
Rajji, Tarek K. [1 ,2 ,3 ]
Barr, Mera S. [1 ,2 ,3 ]
Chen, Robert [4 ]
Daskalakis, Zafiris J. [1 ,2 ,3 ]
Blumberger, Daniel M. [1 ,2 ,3 ]
机构
[1] Ctr Addict & Mental Hlth, Temerty Ctr Therapeut Brain Intervent, Toronto, ON, Canada
[2] Ctr Addict & Mental Hlth, Campbell Family Mental Hlth Res Inst, Toronto, ON, Canada
[3] Univ Toronto, Dept Psychiat, Toronto, ON, Canada
[4] Univ Toronto, Univ Hlth Network, Div Brain Imaging & Behav Syst Neurosci, Toronto Western Res Inst,Dept Med,Div Neurol, Toronto, ON, Canada
基金
美国国家卫生研究院; 加拿大创新基金会; 加拿大自然科学与工程研究理事会; 加拿大健康研究院;
关键词
short-latency afferent inhibition; dorsolateral prefrontal cortex; combined TMS-EEG study; TMS-evoked potentials; TRANSCRANIAL MAGNETIC STIMULATION; INTERVAL CORTICAL INHIBITION; INDEPENDENT COMPONENT ANALYSIS; MILD COGNITIVE IMPAIRMENT; INTRACORTICAL INHIBITION; POSTSYNAPTIC POTENTIALS; PARKINSONS-DISEASE; HIPPOCAMPAL SLICES; ALZHEIMERS-DISEASE; STIMULUS-INTENSITY;
D O I
10.1152/jn.00260.2016
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
A Combined transcranial magnetic stimulation and electroencephalography (TMS-EEG) enables noninvasive neurophysiological investigation of the human cortex. A TMS paradigm of short-latency afferent inhibition (SAI) is characterized by attenuation of the motor-evoked potential (MEP) and modulation of N100 of the TMS-evoked potential (TEP) when TMS is delivered to motor cortex (M1) following median nerve stimulation. SAI is a marker of cholinergic activity in the motor cortex; however, the SAI has not been tested from the prefrontal cortex. We aimed to explore the effect of SAI in dorsolateral prefrontal cortex (DLPFC). SAI was examined in 12 healthy subjects with median nerve stimulation and TMS delivered to M1 and DLPFC at interstimulus intervals (ISIs) relative to the individual N20 latency. SAI in M1 was tested at the optimal ISI of N20 + 2 ms. SAI in DLPFC was investigated at a range of ISI from N20 + 2 to N20 + 20 ms to explore its temporal profile. For SAI in M1, the attenuation of MEP amplitude was correlated with an increase of TEP N100 from the left central area. A similar spatiotemporal neural signature of SAI in DLPFC was observed with a marked increase of N100 amplitude. SAI in DLPFC was maximal at ISI N20 + 4 ms at the left frontal area. These findings establish the neural signature of SAI in DLPFC. Future studies could explore whether DLPFC-SAI is neurophysiological marker of cholinergic dysfunction in cognitive disorders.
引用
收藏
页码:938 / 948
页数:11
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