scholarly journals Slow-oscillatory tACS does not modulate human motor cortical response to repeated plasticity paradigms

2021 ◽  
Author(s):  
Claire Bradley ◽  
Jessica Elliott ◽  
Samuel Dudley ◽  
Genevieve Kieseker ◽  
Jason B Mattingley ◽  
...  

Previous history of activity and learning modulates synaptic plasticity and can lead to saturation of synaptic connections. According to the synaptic homeostasis hypothesis, neural oscillations during slow-wave sleep play an important role in restoring plasticity within a functional range. However, it is not known whether slow-wave oscillations - without the concomitant requirement of sleep - play a causal role in human synaptic homeostasis. Here, slow-oscillatory transcranial alternating current stimulation (tACS, 1Hz, 1mA, 18 minutes) was interleaved between two plasticity-inducing interventions: motor learning, and a paradigm known to induce long-term-potentiation-like plasticity in human motor cortex (paired associative stimulation; PAS). The hypothesis tested was that slow-oscillatory tACS would abolish the expected interference between motor learning and PAS, and facilitate plasticity from successive interventions. Thirty-six participants received sham and active fronto-motor tACS in two separate sessions, along with electroencephalography (EEG) recordings. A further 38 participants received tACS through a control (posterior midline) montage. Using neuro-navigated transcranial magnetic stimulation (TMS) over the left motor cortex, motor evoked potentials (MEPs) were recorded throughout the session. Bayesian statistics were used to quantify evidence for or against the hypothesis of an effect of each intervention on MEP amplitude. As expected, there was converging evidence that motor training increased MEPs. Importantly, we found moderate evidence against an effect of active tACS in restoring PAS plasticity, and no evidence of lasting entrainment of slow-oscillations in the EEG. This suggests that, under the conditions tested here, slow-oscillatory tACS does not modulate synaptic homeostasis in the motor system of awake humans.

2011 ◽  
Vol 4 (3) ◽  
pp. 137-144 ◽  
Author(s):  
Tarek K. Rajji ◽  
Shi-Kai Liu ◽  
Marina V. Frantseva ◽  
Benoit H. Mulsant ◽  
Jessica Thoma ◽  
...  

2019 ◽  
Vol 122 (4) ◽  
pp. 1397-1405 ◽  
Author(s):  
Hiroki Ohashi ◽  
Paul L. Gribble ◽  
David J. Ostry

Motor learning is associated with plasticity in both motor and somatosensory cortex. It is known from animal studies that tetanic stimulation to each of these areas individually induces long-term potentiation in its counterpart. In this context it is possible that changes in motor cortex contribute to somatosensory change and that changes in somatosensory cortex are involved in changes in motor areas of the brain. It is also possible that learning-related plasticity occurs in these areas independently. To better understand the relative contribution to human motor learning of motor cortical and somatosensory plasticity, we assessed the time course of changes in primary somatosensory and motor cortex excitability during motor skill learning. Learning was assessed using a force production task in which a target force profile varied from one trial to the next. The excitability of primary somatosensory cortex was measured using somatosensory evoked potentials in response to median nerve stimulation. The excitability of primary motor cortex was measured using motor evoked potentials elicited by single-pulse transcranial magnetic stimulation. These two measures were interleaved with blocks of motor learning trials. We found that the earliest changes in cortical excitability during learning occurred in somatosensory cortical responses, and these changes preceded changes in motor cortical excitability. Changes in somatosensory evoked potentials were correlated with behavioral measures of learning. Changes in motor evoked potentials were not. These findings indicate that plasticity in somatosensory cortex occurs as a part of the earliest stages of motor learning, before changes in motor cortex are observed. NEW & NOTEWORTHY We tracked somatosensory and motor cortical excitability during motor skill acquisition. Changes in both motor cortical and somatosensory excitability were observed during learning; however, the earliest changes were in somatosensory cortex, not motor cortex. Moreover, the earliest changes in somatosensory cortical excitability predict the extent of subsequent learning; those in motor cortex do not. This is consistent with the idea that plasticity in somatosensory cortex coincides with the earliest stages of human motor learning.


2013 ◽  
Vol 109 (1) ◽  
pp. 89-98 ◽  
Author(s):  
Nigel C. Rogasch ◽  
Zafiris J. Daskalakis ◽  
Paul B. Fitzgerald

Long-interval cortical inhibition (LICI) refers to suppression of neuronal activity following paired-pulse transcranial magnetic stimulation (TMS) with interstimulus intervals (ISIs) between 50 and 200 ms. LICI can be measured either from motor-evoked potentials (MEPs) in small hand muscles or directly from the cortex using concurrent electroencephalography (EEG). However, it remains unclear whether EEG inhibition reflects similar mechanisms to MEP inhibition. Eight healthy participants received single- and paired-pulse TMS (ISI = 100 ms) over the motor cortex. MEPs were measured from a small hand muscle (first dorsal interosseus), whereas early (P30, P60) and late (N100) TMS-evoked cortical potentials (TEPs) were measured over the motor cortex using EEG. Conditioning and test TMS intensities were altered, and modulation of LICI strength was measured using both methods. LICI of MEPs and both P30 and P60 TEPs increased in strength with increasing conditioning intensities and decreased with increasing test intensities. LICI of N100 TEPs remained unchanged across all conditions. In addition, MEP and P30 LICI strength correlated with the slope of the N100 evoked by the conditioning pulse. LICI of early and late TEP components was differentially modulated with altered TMS intensities, suggesting independent underlying mechanisms. LICI of P30 is consistent with inhibition of cortical excitation similar to MEPs, whereas LICI of N100 may reflect presynaptic autoinhibition of inhibitory interneurons. The N100 evoked by the conditioning pulse is consistent with the mechanism responsible for LICI, most likely GABAB-mediated inhibition of cortical activity.


2009 ◽  
Vol 120 (1) ◽  
pp. e61
Author(s):  
I. Delvendahl ◽  
N. Jung ◽  
M. Cronjaeger ◽  
F. Mainberger ◽  
N. Kuhnke ◽  
...  

2014 ◽  
Vol 111 (3) ◽  
pp. 594-601 ◽  
Author(s):  
Behzad Elahi ◽  
William D. Hutchison ◽  
Z. Jeff Daskalakis ◽  
Carolyn Gunraj ◽  
Robert Chen

Associative plasticity is hypothesized to be an important neurophysiological correlate of memory formation and learning with potentials for applications in neurorehabilitation and for the development of new electrophysiological measures to study disorders of cortical plasticity. We hypothesized that the magnitude of the paired associative stimulation (PAS)-induced long-term potentiation (LTP)-like effect depends on the number of pairs in the PAS protocol. We also hypothesized that homeostatic interaction of PAS with subsequent motor learning is related to the magnitude of the PAS-induced LTP-like effect. We studied 10 healthy subjects. In experiment 1a, subjects received 90 (PAS90), 180 (PAS180), or 270 (PAS270) pairs of stimuli, followed by a dynamic motor practice (DMP) 1 h after the end of the PAS protocols. In experiment 1b, the DMP preceded the PAS protocol. In experiment 2, the time course of PAS270 was studied. We found that PAS270 resulted in greater increase in motor evoked potential (MEP) amplitude compared with protocols with fewer pairs of stimuli. Moreover, the interaction between PAS protocols with motor learning differed depending on the number of stimulus pairs used to induce PAS. While DMP alone increased MEP amplitudes, DMP during the LTP-like effects induced by PAS270 led to a long-term depression (LTD)-like effect (homeostatic interaction). This homeostatic interaction did not occur after PAS90 and PAS180. In conclusion, we found a dose-dependent effect of the number of stimulus pairs used in the PAS protocol on cortical plasticity. Homeostatic interaction between PAS and DMP was observed only after PAS270.


2013 ◽  
Vol 109 (12) ◽  
pp. 3060-3066 ◽  
Author(s):  
Martin Sommer ◽  
Milena Rummel ◽  
Christoph Norden ◽  
Holger Rothkegel ◽  
Nicolas Lang ◽  
...  

Our knowledge about the mechanisms of human motor cortex facilitation induced by repetitive transcranial magnetic stimulation (rTMS) is still incomplete. Here we used pharmacological conditioning with carbamazepine, dextrometorphan, lorazepam, and placebo to elucidate the type of plasticity underlying this facilitation, and to probe if mechanisms reminiscent of long-term potentiation are involved. Over the primary motor cortex of 10 healthy subjects, we applied biphasic rTMS pulses of effective posterior current direction in the brain. We used six blocks of 200 pulses at 5-Hz frequency and 90% active motor threshold intensity and controlled for corticospinal excitability changes using motor-evoked potential (MEP) amplitudes and latencies elicited by suprathreshold pulses before, in between, and after rTMS. Target muscle was the dominant abductor digiti minimi muscle; we coregistered the dominant extensor carpi radialis muscle. We found a lasting facilitation induced by this type of rTMS. The GABAergic medication lorazepam and to a lesser extent the ion channel blocker carbamazepine reduced the MEP facilitation after biphasic effective posteriorly oriented rTMS, whereas the N-methyl-d-aspartate receptor-antagonist dextrometorphan had no effect. Our main conclusion is that the mechanism of the facilitation induced by biphasic effective posterior rTMS is more likely posttetanic potentiation than long-term potentiation. Additional findings were prolonged MEP latency under carbamazepine, consistent with sodium channel blockade, and larger MEP amplitudes from extensor carpi radialis under lorazepam, suggesting GABAergic involvement in the center-surround balance of excitability.


2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Prachaya Srivanitchapoom ◽  
Jung E. Park ◽  
Nivethida Thirugnanasambandam ◽  
Pattamon Panyakaew ◽  
Vesper Fe Marie Ramos ◽  
...  

Introduction.Paired associative stimulation (PAS) is an established technique to investigate synaptic plasticity in the human motor cortex (M1). Classically, to induce long-term depression- (LTD-) or long-term potentiation-like effects in the human M1, studies have used low frequency and long duration trains of PAS. In the present study, we explored an LTD-like effect using very short duration and low frequency ofPAS10 msprotocols in human M1.Methods.Six protocols of low frequencyPAS10 ms(ranging from 0.2 Hz to 1 Hz) were investigated with very short durations of 1 and 2 minutes stimulation. Six healthy volunteers were included in each protocol. We obtained motor-evoked potentials from right abductor pollicis brevis muscle before and after applyingPAS10 msup to 30 minutes. After we foundPAS10 msprotocol which induced an LTD-like effect, we tested that protocol on additional 5 subjects.Results.One-way repeated-measures ANOVA showed that only the group of 1-minute stimulation of 0.25 Hz induced an LTD-like effect. When adding the additional subjects, the effect remained and lasted for 30 minutes.Conclusion.Low frequency and very short duration ofPAS10 mspotentially induced an LTD-like effect in human M1. With further verification, this method might be useful for research relating to synaptic plasticity by reducing the duration of study and minimizing subject discomfort.


2003 ◽  
Vol 89 (5) ◽  
pp. 2339-2345 ◽  
Author(s):  
Alexander Wolters ◽  
Friedhelm Sandbrink ◽  
Antje Schlottmann ◽  
Erwin Kunesch ◽  
Katja Stefan ◽  
...  

Synaptic plasticity is conspicuously dependent on the temporal order of the pre- and postsynaptic activity. Human motor cortical excitability can be increased by a paired associative stimulation (PAS) protocol. Here we show that it can also be decreased by minimally changing the interval between the two associative stimuli. Corticomotor excitability of the abductor pollicis brevis (APB) representation was tested before and after repetitively pairing of single right median nerve simulation with single pulse transcranial magnetic stimulation (TMS) delivered over the optimal site for activation of the contralateral APB. Following PAS, depression of TMS-evoked motor-evoked potentials (MEPs) was induced only when the median nerve stimulation preceded the TMS pulse by 10 ms, while enhancement of cortical excitability was induced using an interstimulus interval of 25 ms, suggesting an important role of the sequence of cortical events triggered by the two stimulation modalities. Experiments using F-wave studies and electrical brain stem stimulation indicated that the site of the plastic changes underlying the decrease of MEP amplitudes following PAS (10 ms) was within the motor cortex. MEP amplitudes remained depressed for approximately 90 min. The decrease of MEP amplitudes was blocked when PAS(10 ms) was performed under the influence of dextromethorphan, an N-methyl-d-aspartate-receptor antagonist, or nimodipine, an L-type voltage-gated calcium-channel antagonist. The physiological profile of the depression of human motor cortical excitability following PAS(10 ms) suggests long-term depression of synaptic efficacy to be involved. Together with earlier findings, this study suggests that strict temporal Hebbian rules govern the induction of long-term potentiation/long-term depression-like phenomena in vivo in the human primary motor cortex.


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