4.4 Article

Paired Associative Stimulation Induces Change in Presynaptic Inhibition of Ia Terminals in Wrist Flexors in Humans

Journal

JOURNAL OF NEUROPHYSIOLOGY
Volume 104, Issue 2, Pages 755-764

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.00761.2009

Keywords

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Funding

  1. National Institutes of Health, National Institute of Neurological Disorders and Stroke
  2. Fondation pour la Recherche Medicale
  3. Intramural National Institutes of Health
  4. Swiss National Funds [PBSKB-104264]
  5. Swiss Parkinson Society

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Lamy J-C, Russmann H, Shamim EA, Meunier S, Hallett M. Paired associative stimulation induces change in presynaptic inhibition of Ia terminals in wrist flexors in humans. J Neurophysiol 104: 755-764, 2010. First published June 10, 2010; doi:10.1152/jn.00761.2009. Enhancements in the strength of corticospinal projections to muscles are induced in conscious humans by paired associative stimulation (PAS) to the motor cortex. Although most of the previous studies support the hypothesis that the increase of the amplitude of motor evoked potentials (MEPs) by PAS involves long-term potentiation (LTP)-like mechanism in cortical synapses, changes in spinal excitability after PAS have been reported, suggestive of parallel modifications in both cortical and spinal excitability. In a first series of experiments (experiment 1), we confirmed that both flexor carpi radialis (FCR) MEPs and FCR H reflex recruitment curves are enhanced by PAS. To elucidate the mechanism responsible for this change in the H reflex amplitude, we tested, using the same subjects, the hypothesis that enhanced H reflexes are caused by a down-regulation of the efficacy of mechanisms controlling Ia afferent discharge, including presynaptic Ia inhibition and postactivation depression. To address this question, amounts of both presynaptic Ia inhibition of FCR Ia terminals (D1 and D2 inhibitions methods; experiment 2) and postactivation depression (experiment 3) were determined before and after PAS. Results showed that PAS induces a significant decrease of presynaptic Ia inhibition of FCR terminals, which was concomitant with the facilitation of the H reflex. Postactivation depression was unaffected by PAS. It is argued that enhancement of segmental excitation by PAS relies on a selective effect of PAS on the interneurons controlling presynaptic inhibition of Ia terminals.

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