Chapter 3 Long-term potentiation (LTP)-like plasticity and learning in human motor cortex – investigations with transcranial magnetic stimulation (TMS)

Author(s):  
Ulf Ziemann ◽  
Tihomir V. Ilić ◽  
Patrick Jung
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.


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

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

2008 ◽  
Vol 39 (01) ◽  
Author(s):  
I Delvendahl ◽  
N Jung ◽  
M Cronjaeger ◽  
F Mainberger ◽  
N Kuhnke ◽  
...  

Cortex ◽  
2017 ◽  
Vol 88 ◽  
pp. 32-41 ◽  
Author(s):  
Martin V. Sale ◽  
Abbey S. Nydam ◽  
Jason B. Mattingley

2008 ◽  
Vol 39 (01) ◽  
Author(s):  
I Delvendahl ◽  
N Jung ◽  
N Kuhnke ◽  
M Cronjaeger ◽  
P Noellke ◽  
...  

1995 ◽  
Vol 73 (2) ◽  
pp. 218-222 ◽  
Author(s):  
M. C. Ridding ◽  
J. C Rothwell

Transcranial magnetic stimulation over the motor cortex was used to construct a map of the effective sites on the scalp from which short-latency electromyogram responses could be evoked in muscles proximal to either an amputation stump (two subjects) or an ischemically anesthetized forearm (two subjects). At rest, the maps were larger and the responses bigger when stimulating contralateral to the amputated arm or after anesthesia than they were in the intact arm or before anesthesia. However, this difference disappeared when the maps were constructed during a small tonic voluntary contraction of the target muscle. We conclude that reorganisation of the corticospinal projection to a muscle at rest may no longer be present during activity. If so, this calls into question the possible functional benefits of such reorganisation in the control of movement after peripheral damage.Key words: motor cortex, magnetic stimulation, amputation, ischemia.


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