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Cited by 423

The DOI matches its Crossref record; 55 of the 55 references it cites were found in a registry or an index.

Modulation of human corticomotor excitability by somatosensory input

Open access
Kaelin‐Lang, Alain, Luft, Andreas R., Sawaki, Lumy, Burstein, Aaron H., Sohn, Young H., Cohen, Leonardo G.·2002·The Journal of Physiology
DOI 10.1113/jphysiol.2001.012801
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Abstract

In humans, somatosensory stimulation results in increased corticomotoneuronal excitability to the stimulated body parts. The purpose of this study was to investigate the underlying mechanisms. We recorded motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) from abductor pollicis brevis (APB), first dorsal interosseous (FDI), and abductor digiti minimi (ADM) muscles. MEP amplitudes, recruitment curves (RC), intracortical inhibition (ICI), intracortical facilitation (ICF), resting (rMT) and active motor thresholds (aMT) were recorded before and after a 2‐h period of ulnar nerve electrical stimulation at the wrist. Somatosensory input was monitored by recording somatosensory evoked potentials. To differentiate excitability changes at cortical vs. subcortical sites, we recorded supramaximal peripheral M‐responses and MEPs to brainstem electrical stimulation (BES). In order to investigate the involvement of GABAergic mechanisms, we studied the influence of lorazepam (LZ) (a GABA A receptor agonist) relative to that of dextromethorphan (DM) (an NMDA receptor antagonist) and placebo in a double‐blind design. We found that somatosensory stimulation increased MEP amplitudes to TMS only in the ADM, confirming a previous report. This effect was blocked by LZ but not by either DM or placebo and lasted between 8 and 20 min in the absence of (i) changes in MEPs elicited by BES, (ii) amplitudes of early somatosensory‐evoked potentials or (iii) M‐responses. We conclude that somatosensory stimulation elicited a focal increase in corticomotoneuronal excitability that outlasts the stimulation period and probably occurs at cortical sites. The antagonistic effect of LZ supports the hypothesis of GABAergic involvement as an operating mechanism.

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Metadata

Authors
Kaelin‐Lang, A., Luft, A. R., Sawaki, L., Burstein, A. H., Sohn, Y. H., & Cohen, L. G.
Venue
The Journal of Physiology
Publisher
Wiley
Published
2002-04
Volume
540
Issue
2
Pages
623-633
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
DOI
10.1113/jphysiol.2001.012801
OpenAlex
W2129348555
Cited by
423
References
55
FWCI
9.03
Type
journal article
Language
en
Open access
green

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