TY - JOUR
T1 - Facilitation of Early and Middle Latency SEP after tDCS of M1
T2 - No Evidence of Primary Somatosensory Homeostatic Plasticity
AU - Zolezzi, Daniela M.
AU - Larsen, Dennis B.
AU - Zamorano, Anna M.
AU - Graven-Nielsen, Thomas
PY - 2024/7/23
Y1 - 2024/7/23
N2 - Homeostatic plasticity is a mechanism that stabilizes cortical excitability within a physiological range. Most homeostatic plasticity protocols have primed and tested the homeostatic response of the primary motor cortex (M1). This study investigated if a homeostatic response could be recorded from the primary sensory cortex (S1) after inducing homeostatic plasticity in M1. In 31 healthy participants, homeostatic plasticity was induced over M1 with a priming and testing block of transcranial direct current stimulation (tDCS) in two different sessions (anodal and cathodal). S1 excitability was assessed by early (N20, P25) and middle-latency (N33-P45) somatosensory evoked potentials (SEP) extracted from 4 electrodes (CP5, CP3, P5, P3). Baseline and post-measures (post-priming, 0-min, 10-min, and 20-min after homeostatic induction) were taken. Anodal M1 homeostatic plasticity induction significantly facilitated the N20-P25, P45 peak, and N33-P45 early SEP components up to 20-min post-induction, without any indication of a homeostatic response (i.e., reduced SEP). Cathodal homeostatic induction did not induce any significant effect on early or middle latency SEPs. M1 homeostatic plasticity induction by anodal stimulation protocol to the primary motor cortex did not induce a homeostatic response in SEPs.
AB - Homeostatic plasticity is a mechanism that stabilizes cortical excitability within a physiological range. Most homeostatic plasticity protocols have primed and tested the homeostatic response of the primary motor cortex (M1). This study investigated if a homeostatic response could be recorded from the primary sensory cortex (S1) after inducing homeostatic plasticity in M1. In 31 healthy participants, homeostatic plasticity was induced over M1 with a priming and testing block of transcranial direct current stimulation (tDCS) in two different sessions (anodal and cathodal). S1 excitability was assessed by early (N20, P25) and middle-latency (N33-P45) somatosensory evoked potentials (SEP) extracted from 4 electrodes (CP5, CP3, P5, P3). Baseline and post-measures (post-priming, 0-min, 10-min, and 20-min after homeostatic induction) were taken. Anodal M1 homeostatic plasticity induction significantly facilitated the N20-P25, P45 peak, and N33-P45 early SEP components up to 20-min post-induction, without any indication of a homeostatic response (i.e., reduced SEP). Cathodal homeostatic induction did not induce any significant effect on early or middle latency SEPs. M1 homeostatic plasticity induction by anodal stimulation protocol to the primary motor cortex did not induce a homeostatic response in SEPs.
KW - homeostatic plasticity
KW - primary motor cortex
KW - primary sensory cortex
KW - somatosensory evoked potentials
KW - transcranial direct current stimulation
UR - http://www.scopus.com/inward/record.url?scp=85195294616&partnerID=8YFLogxK
U2 - 10.1016/j.neuroscience.2024.05.001
DO - 10.1016/j.neuroscience.2024.05.001
M3 - Journal article
C2 - 38735429
AN - SCOPUS:85195294616
SN - 0306-4522
VL - 551
SP - 143
EP - 152
JO - Neuroscience
JF - Neuroscience
ER -