Format

Send to

Choose Destination
Sci Rep. 2019 Aug 8;9(1):11543. doi: 10.1038/s41598-019-47932-9.

Interaction between repetition suppression in motor activation and long-interval intracortical inhibition.

Author information

1
Department of Applied Physics, University of Eastern Finland, Kuopio, Finland. shohreh.kariminezhad@uef.fi.
2
Department of Clinical Neurophysiology, Kuopio University Hospital, Kuopio, Finland. shohreh.kariminezhad@uef.fi.
3
Nexstim Plc, Helsinki, Finland.
4
Department of Clinical Neurophysiology, Kuopio University Hospital, Kuopio, Finland.
5
Department of Clinical Radiology, Kuopio University Hospital, Kuopio, Finland.
6
Department of Applied Physics, University of Eastern Finland, Kuopio, Finland.

Abstract

Repetition suppression (RS) is the adaptation of the neural activity in response to a repeated external stimulus. It has been proposed that RS occurs at the thalamo-cortical level, hence activating a feedback loop to the cortex in order to counteract with the repeated motor cortical activation. In this study, to elucidate the common modulators between the RS and the inhibitory/facilitatory cortical networks, two TMS paradigms were applied, i.e. the characteristic long-interval intracortical inhibition (LICI) and the I1-wave timed short-interval intracortical facilitation (SICF). Since LICI is a local intracortical inhibitory phenomenon affecting cortical excitation over a long interval like the RS, the interaction between RS and LICI was tested. As the I1-wave timed SICF is likely not affected by inhibitory modulation, the appearance of the RS with respect to SICF was investigated. Non-linear interaction between LICI and RS was observed, while I1-wave timed SICF facilitated all MEP responses of RS by a common offset still preserving the RS. These findings implicate that the underlying mechanism for the observed interaction is likely contributed to the activation of the negative thalamo-cortical feedback loop represented by the RS, most likely at the cortical level.

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center