期刊
JOURNAL OF NEUROPHYSIOLOGY
卷 116, 期 3, 页码 938-948出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.00260.2016
关键词
short-latency afferent inhibition; dorsolateral prefrontal cortex; combined TMS-EEG study; TMS-evoked potentials
资金
- Temerty Centre for Therapeutic Brain Intervention
- Campbell Family Research Institute through the Centre for Addiction and Mental Health (CAMH) Foundation
- Canada Foundation for Innovation
- CAMH Foundation
- Canadian Institutes of Health Research (CIHR)-Dystonia Medical Research Foundation
- NARSAD
- Slaight Family Centre for Youth in Transition at the CAMH
- Natural Sciences and Engineering Research Council of Canada (NSERC)
- Ontario Brain Institute (OBI)
- Brain Canada
- Brain and Behavior Research Foundation
- CIHR
- Ontario Ministry of Health and Long-Term Care
- Ontario Ministry of Research and Innovation
- US National Institutes of Health (NIH)
- W. Garfield Weston Foundation
- Brain and Behaviour Research Foundation
- Temerty family and Grant family through the CAMH Foundation
- Campbell Institute
- Sepracor
- AstraZeneca
- US NIH
- Temerty family through the CAMH Foundation
- Campbell Research Institute
- Brainsway Limited
- Ontario Mental Health (OMH) Foundation
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.
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