ePoster

MODULATION OF INTERHEMISPHERIC INHIBITION WITHIN THE PRIMARY SOMATOSENSORY CORTEX BY TRANSCRANIAL STATIC MAGNETIC STIMULATION

Yuki Tanakaand 7 co-authors

Graduate School of Health Sciences, Aomori University of Health and Welfare

FENS Forum 2026 (2026)
Barcelona, Spain
Board PS04-08PM-479

Presentation

Date TBA

Board: PS04-08PM-479

Poster preview

MODULATION OF INTERHEMISPHERIC INHIBITION WITHIN THE PRIMARY SOMATOSENSORY CORTEX BY TRANSCRANIAL STATIC MAGNETIC STIMULATION poster preview

Event Information

Poster Board

PS04-08PM-479

Abstract

Transcranial static magnetic field stimulation (tSMS) is a non-invasive brain stimulation (NIBS) technique that reduces cortical excitability. Currently, its effects on interhemispheric inhibition (IHI) within the primary somatosensory cortex (S1) remain unclear. In the present study, we addressed this unsolved question using paired somatosensory evoked potential (pSEP) paradigm. Twenty-five healthy young adults received either tSMS or sham stimulation over the right S1 for 20 min. Somatosensory evoked potentials were elicited by a test stimulus to the right median nerve, preceded by a conditioning stimulus (CS) to the left median nerve with a 10-ms interstimulus interval. Recordings were obtained at baseline, immediately after stimulation, and 20 min post-stimulation. In addition to the N20 and P25 components, high-frequency oscillations (HFOs) were extracted and separated into early and late HFOs relative to the N20 peak latency. The N20 and P25 components are considered to reflect activity in Brodmann area 3b of the S1, while early and late HFOs are thought to reflect action potentials of thalamocortical fibers and GABAergic interneuron activity within the S1, respectively. TSMS significantly attenuated CS-induced suppression of late HFO amplitudes in the left S1 immediately after stimulation, whereas no significant changes were observed in the other components. These findings suggest that tSMS over the S1 preferentially modulates transcallosal inhibitory interactions mediated by intracortical GABAergic circuits.

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