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Repetitive Activation of the Corticospinal Pathway by Means of rTMS may Reduce the Efficiency of Corticomotoneuronal Synapses

Taube, Wolfgang ; Leukel, Christian ; Nielsen, Jens Bo ; Lundbye-Jensen, Jesper

In: Cerebral Cortex, 2015, vol. 25, no. 6, p. 1629-1637

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    Title
    • Repetitive Activation of the Corticospinal Pathway by Means of rTMS may Reduce the Efficiency of Corticomotoneuronal Synapses
    Author
    • Taube, Wolfgang. Department of Medicine, Movement and Sport Science, University of Fribourg, 1700 Fribourg, Switzerland
    • Leukel, Christian. Department of Medicine, Movement and Sport Science, University of Fribourg, 1700 Fribourg, Switzerland
    • Nielsen, Jens Bo. Department of Nutrition, Exercise and Sports
    • Lundbye-Jensen, Jesper. Department of Nutrition, Exercise and Sports
    Document Type
    • Postprint
    Language
    • English
    Published in
    • Cerebral Cortex, 2015, vol. 25, no. 6, p. 1629-1637. Oxford University Press
    Other Version
    OAI-PMH Identifier
    • oai:doc.rero.ch:295311
    Summary
    Low-frequency rTMS applied to the primary motor cortex (M1) may produce depression of motor-evoked potentials (MEPs). This depression is commonly assumed to reflect changes in cortical circuits. However, little is known about rTMS-induced effects on subcortical circuits. Therefore, the present study aimed to clarify whether rTMS influences corticospinal transmission by altering the efficiency of corticomotoneuronal (CM) synapses. The corticospinal transmission to soleus α-motoneurons was evaluated through conditioning of the soleus H-reflex by magnetic stimulation of either M1 (M1-conditioning) or the cervicomedullary junction (CMS-conditioning). The first facilitation of the H-reflex (early facilitation) was determined after M1- and CMS-conditioning. Comparison of the early facilitation before and after 20-min low-frequency (1 Hz) rTMS revealed suppression with M1- (−17 ± 4%; P = 0.001) and CMS-conditioning (−6 ± 2%; P = 0.04). The same rTMS protocol caused a significant depression of compound MEPs, whereas amplitudes of H-reflex and M-wave remained unaffected, indicating a steady level of motoneuronal excitability. Thus, the effects of rTMS are likely to occur at a premotoneuronal site—either at M1 and/or the CM synapse. As the early facilitation reflects activation of direct CM projections, the most likely site of action is the synapse of the CM neurons onto spinal motoneurons