Short-latency afferent inhibition from the motor and dorsolateral prefrontal cortex in healthy subjects: a combined TMS–EEG study

2015 ◽  
Vol 8 (2) ◽  
pp. 316 ◽  
Author(s):  
Yoshihiro Noda ◽  
Robin F. Cash ◽  
Luis Garcia Dominguez ◽  
Faranak Farzan ◽  
Tarek K. Rajji ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Healthy Subjects ◽  
Dorsolateral Prefrontal Cortex ◽  
Short Latency ◽  
Short Latency Afferent Inhibition ◽  
Afferent Inhibition ◽  
Dorsolateral Prefrontal

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

2016 ◽  
Vol 116 (3) ◽  
pp. 938-948 ◽  
Author(s):  
Yoshihiro Noda ◽  
Robin F. H. Cash ◽  
Reza Zomorrodi ◽  
Luis Garcia Dominguez ◽  
Faranak Farzan ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Motor Cortex ◽  
Nerve Stimulation ◽  
Dorsolateral Prefrontal Cortex ◽  
Evoked Potential ◽  
Short Latency Afferent Inhibition ◽  
Afferent Inhibition ◽  
Median Nerve Stimulation ◽  
Dorsolateral Prefrontal ◽  
Neural Signature

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.

scholarly journals Mechanistic link between right prefrontal cortical activity and anxious arousal revealed using transcranial magnetic stimulation in healthy subjects

2019 ◽  
Vol 45 (4) ◽  
pp. 694-702 ◽  
Author(s):  
Nicholas L. Balderston ◽  
Emily M. Beydler ◽  
Camille Roberts ◽  
Zhi-De Deng ◽  
Thomas Radman ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Transcranial Magnetic Stimulation ◽  
Healthy Subjects ◽  
Magnetic Stimulation ◽  
Dorsolateral Prefrontal Cortex ◽  
Subcortical Structures ◽  
Prefrontal Cortical ◽  
Dorsolateral Prefrontal ◽  
Before And After ◽  
The Right

AbstractMuch of the mechanistic research on anxiety focuses on subcortical structures such as the amygdala; however, less is known about the distributed cortical circuit that also contributes to anxiety expression. One way to learn about this circuit is to probe candidate regions using transcranial magnetic stimulation (TMS). In this study, we tested the involvement of the dorsolateral prefrontal cortex (dlPFC), in anxiety expression using 10 Hz repetitive TMS (rTMS). In a within-subject, crossover experiment, the study measured anxiety in healthy subjects before and after a session of 10 Hz rTMS to the right dorsolateral prefrontal cortex (dlPFC). It used threat of predictable and unpredictable shock to induce anxiety and anxiety potentiated startle to assess anxiety. Counter to our hypotheses, results showed an increase in anxiety-potentiated startle following active but not sham rTMS. These results suggest a mechanistic link between right dlPFC activity and physiological anxiety expression. This result supports current models of prefrontal asymmetry in affect, and lays the groundwork for further exploration into the cortical mechanisms mediating anxiety, which may lead to novel anxiety treatments.

Sign in / Sign up

Export Citation Format

Share Document