Activation of the Supplementary Motor Areas Enhances Spinal Reciprocal Inhibition in Healthy Individuals

Ryo Hirabayashi,Mutsuaki Edama,Sho Kojima,Hideaki Onishi

doi:10.3390/brainsci10090587

Ryo Hirabayashi, Mutsuaki Edama + Show 2 more

Open Access

https://doi.org/10.3390/brainsci10090587

Copy DOI

Journal: Brain sciences	Publication Date: Aug 24, 2020
Citations: 8	License type: CC BY 4.0

Affiliation: Niigata University of Health and Welfare

Abstract

The supplementary motor area (SMA) may modulate spinal reciprocal inhibition (RI) because the descending input from the SMA is coupled to interneurons in the spinal cord via the reticulospinal tract. Our study aimed to verify whether the anodal transcranial direct current stimulation (anodal-tDCS) of the SMA enhances RI. Two tDCS conditions were used: the anodal stimulation (anodal-tDCS) and sham stimulation (sham-tDCS) conditions. To measure RI, there were two conditions: one with the test stimulus (alone) and the other with the conditioning-test stimulation intervals (CTIs), including 2 ms and 20 ms. RI was calculated at multiple time points: before the tDCS intervention (Pre); at 5 (Int 5) and 10 min; and immediately after (Post 0); and at 5, 10 (Post 10), 15, and 20 min after the intervention. In anodal-tDCS, the amplitude values of H-reflex were significantly reduced for a CTI of 2 ms at Int 5 to Post 0, and a CTI of 20 ms at Int 5 to Pot 10 compared with Pre. Stimulation of the SMA with anodal-tDCS for 15 min activated inhibitory interneurons in RIs by descending input from the reticulospinal tract via cortico–reticulospinal projections. The results showed that 15 min of anodal-tDCS in the SMA enhanced and sustained RI in healthy individuals.

Highlights

Dysfunction of neurons of the upper motor system [1,2,3], spinal cord injury [4], and aging [5,6,7,8,9,10]disrupt smooth joint movement owing to excessive simultaneous activation (ESA) of antagonist muscles, decreasing exercise performance
These pathways include disynaptic Ia reciprocal inhibition (RI) (DRI) that directly links to spinal anterior horn cells (SAHC) of antagonist muscles [14,15] and presynaptic short (D1 inhibition) and long (D2 inhibition) latency inhibition pathways mediated by primary afferent depolarization (PAD)
The results in the current study demonstrated that in comparison with single stimuli, H-reflex amplitude values were significantly reduced at conditioning-test stimulation intervals (CTIs) of 2 and 20 ms for all transcranial direct current stimulation (tDCS) conditions

Summary

Introduction

Dysfunction of neurons of the upper motor system [1,2,3], spinal cord injury [4], and aging [5,6,7,8,9,10]disrupt smooth joint movement owing to excessive simultaneous activation (ESA) of antagonist muscles, decreasing exercise performance. During joint exercises based on repetitive and quick actions, ESA causes inhibition of smooth joint movement and triggers fatigue in the agonist muscle [13]. The mechanism underlying these ESAs is the repression of interneurons of reciprocal inhibition (RI) by Renshaw cells [1,2,3]. RI is an essential function for normal joint movement, balance and gait, and involves three inhibitory pathways These pathways include disynaptic Ia RI (DRI) that directly links to spinal anterior horn cells (SAHC) of antagonist muscles [14,15] and presynaptic short (D1 inhibition) and long (D2 inhibition) latency inhibition pathways mediated by primary afferent depolarization (PAD).

Objectives

Discussion

Conclusion