LTD-like plasticity of the human primary motor cortex can be reversed by γ-tACS.
Adult
Evoked Potentials, Motor
/ physiology
Female
Humans
Inhibition, Psychological
Interneurons
/ physiology
Long-Term Synaptic Depression
/ physiology
Male
Motor Cortex
/ physiology
Neuronal Plasticity
/ physiology
Transcranial Direct Current Stimulation
/ methods
Transcranial Magnetic Stimulation
/ methods
Beta
Gamma
Plasticity
TMS
cTBS
tACS
Journal
Brain stimulation
ISSN: 1876-4754
Titre abrégé: Brain Stimul
Pays: United States
ID NLM: 101465726
Informations de publication
Date de publication:
Historique:
received:
20
01
2019
revised:
19
06
2019
accepted:
28
06
2019
pubmed:
11
7
2019
medline:
25
2
2020
entrez:
11
7
2019
Statut:
ppublish
Résumé
Cortical oscillatory activities play a role in regulating several brain functions in humans. However, whether motor resonant oscillations (i.e. β and γ) modulate long-term depression (LTD)-like plasticity of the primary motor cortex (M1) is still unclear. To address this issue, we combined transcranial alternating current stimulation (tACS), a technique able to entrain cortical oscillations, with continuous theta burst stimulation (cTBS), a transcranial magnetic stimulation (TMS) protocol commonly used to induce LTD-like plasticity in M1. Motor evoked potentials (MEPs) elicited by single-pulse TMS, short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF) were evaluated before and 5, 15 and 30 min after cTBS alone or cTBS delivered during β-tACS (cTBS-β) or γ-tACS (cTBS-γ). Moreover, we tested the effects of β-tACS (alone) on short-latency afferent inhibition (SAI) and γ-tACS on SICI in order to verify whether tACS-related interneuronal modulation contributes to the effects of tACS-cTBS co-stimulation. cTBS-γ turned the expected after-effects of cTBS from inhibition to facilitation. By contrast, responses to cTBS-β were similar to those induced by cTBS alone. β- and γ-tACS did not change MEPs evoked by single-pulse TMS. β-tACS reduced SAI and γ-tACS reduced SICI. However, the degree of γ-tACS-induced modulation of SICI did not correlate with the effects of cTBS-γ. γ-tACS reverses cTBS-induced plasticity of the human M1. γ-oscillations may therefore regulate LTD-like plasticity mechanisms.
Sections du résumé
BACKGROUND
Cortical oscillatory activities play a role in regulating several brain functions in humans. However, whether motor resonant oscillations (i.e. β and γ) modulate long-term depression (LTD)-like plasticity of the primary motor cortex (M1) is still unclear.
OBJECTIVE
To address this issue, we combined transcranial alternating current stimulation (tACS), a technique able to entrain cortical oscillations, with continuous theta burst stimulation (cTBS), a transcranial magnetic stimulation (TMS) protocol commonly used to induce LTD-like plasticity in M1.
METHODS
Motor evoked potentials (MEPs) elicited by single-pulse TMS, short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF) were evaluated before and 5, 15 and 30 min after cTBS alone or cTBS delivered during β-tACS (cTBS-β) or γ-tACS (cTBS-γ). Moreover, we tested the effects of β-tACS (alone) on short-latency afferent inhibition (SAI) and γ-tACS on SICI in order to verify whether tACS-related interneuronal modulation contributes to the effects of tACS-cTBS co-stimulation.
RESULTS
cTBS-γ turned the expected after-effects of cTBS from inhibition to facilitation. By contrast, responses to cTBS-β were similar to those induced by cTBS alone. β- and γ-tACS did not change MEPs evoked by single-pulse TMS. β-tACS reduced SAI and γ-tACS reduced SICI. However, the degree of γ-tACS-induced modulation of SICI did not correlate with the effects of cTBS-γ.
CONCLUSION
γ-tACS reverses cTBS-induced plasticity of the human M1. γ-oscillations may therefore regulate LTD-like plasticity mechanisms.
Identifiants
pubmed: 31289014
pii: S1935-861X(19)30287-6
doi: 10.1016/j.brs.2019.06.029
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1490-1499Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.