Spinal inhibition of descending command to soleus motoneurons is removed prior to dorsiflexion

Research output: Contribution to journalJournal articleResearchpeer-review

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Spinal inhibition of descending command to soleus motoneurons is removed prior to dorsiflexion. / Geertsen, Svend Sparre; van de Ruit, Mark; Grey, Michael James; Nielsen, Jens Bo.

In: Journal of Physiology, Vol. 589, No. 23, 2011, p. 5819-5831.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Geertsen, SS, van de Ruit, M, Grey, MJ & Nielsen, JB 2011, 'Spinal inhibition of descending command to soleus motoneurons is removed prior to dorsiflexion', Journal of Physiology, vol. 589, no. 23, pp. 5819-5831. https://doi.org/10.1113/jphysiol.2011.214387

APA

Geertsen, S. S., van de Ruit, M., Grey, M. J., & Nielsen, J. B. (2011). Spinal inhibition of descending command to soleus motoneurons is removed prior to dorsiflexion. Journal of Physiology, 589(23), 5819-5831. https://doi.org/10.1113/jphysiol.2011.214387

Vancouver

Geertsen SS, van de Ruit M, Grey MJ, Nielsen JB. Spinal inhibition of descending command to soleus motoneurons is removed prior to dorsiflexion. Journal of Physiology. 2011;589(23):5819-5831. https://doi.org/10.1113/jphysiol.2011.214387

Author

Geertsen, Svend Sparre ; van de Ruit, Mark ; Grey, Michael James ; Nielsen, Jens Bo. / Spinal inhibition of descending command to soleus motoneurons is removed prior to dorsiflexion. In: Journal of Physiology. 2011 ; Vol. 589, No. 23. pp. 5819-5831.

Bibtex

@article{4feb175f595049e7a7f4d3f625bc2159,
title = "Spinal inhibition of descending command to soleus motoneurons is removed prior to dorsiflexion",
abstract = "It has recently been demonstrated that soleus motor evoked potentials (MEPs) are facilitated prior to the onset of dorsiflexion. The purpose of this study was to examine if this could be explained by removal of spinal inhibition of the descending command to soleus motoneurons. To test this, we investigated how afferent inputs from the tibialis anterior muscle modulate the corticospinal activation of soleus spinal motoneurons at rest, during static contraction and prior to movement. MEPs activated by transcranial magnetic stimulation (TMS) and Hoffmann-reflexes (H-reflexes) activated by electrical stimulation of the posterior tibial nerve (PTN) were conditioned by prior stimulation of the common peroneal nerve (CPN) at a variety of conditioning-test (CT) intervals.MEPs in the precontracted soleus muscle were inhibited when the TMS pulse was preceded by CPN stimulation with a CT interval of 35 ms, and they were facilitated for CT intervals of 50-55 ms. A similar inhibition of the soleus H-reflex was not observed. To investigate which descending pathways might be responsible for the afferent-evoked inhibition and facilitation, we examined the effect of CPN stimulation on short-latency facilitation (SLF) and long-latency facilitation (LLF) of the soleus H-reflex induced by a subthreshold TMS-pulse at different CT intervals. SLF is known to reflect the excitability of the fastest conducting, corticomotoneuronal, cells whereas LLF is believed to be caused by more indirect descending pathways. At CT intervals of 40-45 ms, the LLF was significantly more inhibited compared to the SLF when taking the effect on the H-reflex into account. Finally, we investigated how the CPN-induced inhibition and facilitation of the soleus MEP were modulated prior to dorsiflexion. Whereas the late facilitation (CT interval: 55 ms) was similar prior to dorsiflexion and at rest, no inhibition could be evoked at the earlier latency (CT interval: 35 ms) prior to onset of dorsiflexion.The observation that the CPN-induced inhibition of soleus MEPs disappears prior to onset of dorsiflexion may explain why soleus MEPs are facilitated prior to onset of dorsiflexion contraction. A possible mechanism involves the removal of inhibition of the descending command to the motoneurons at a spinal interneuronal level because the inhibition was seen in LLF and not in SLF and the MEP-inhibition was not observed in the H-reflex. The data illustrate that spinal interneuronal pathways modify descending commands to human spinal motoneurons and influence the size of MEPs elicited by TMS.",
author = "Geertsen, {Svend Sparre} and {van de Ruit}, Mark and Grey, {Michael James} and Nielsen, {Jens Bo}",
note = "CURIS 2011 5200 121",
year = "2011",
doi = "10.1113/jphysiol.2011.214387",
language = "English",
volume = "589",
pages = "5819--5831",
journal = "The Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",
number = "23",

}

RIS

TY - JOUR

T1 - Spinal inhibition of descending command to soleus motoneurons is removed prior to dorsiflexion

AU - Geertsen, Svend Sparre

AU - van de Ruit, Mark

AU - Grey, Michael James

AU - Nielsen, Jens Bo

N1 - CURIS 2011 5200 121

PY - 2011

Y1 - 2011

N2 - It has recently been demonstrated that soleus motor evoked potentials (MEPs) are facilitated prior to the onset of dorsiflexion. The purpose of this study was to examine if this could be explained by removal of spinal inhibition of the descending command to soleus motoneurons. To test this, we investigated how afferent inputs from the tibialis anterior muscle modulate the corticospinal activation of soleus spinal motoneurons at rest, during static contraction and prior to movement. MEPs activated by transcranial magnetic stimulation (TMS) and Hoffmann-reflexes (H-reflexes) activated by electrical stimulation of the posterior tibial nerve (PTN) were conditioned by prior stimulation of the common peroneal nerve (CPN) at a variety of conditioning-test (CT) intervals.MEPs in the precontracted soleus muscle were inhibited when the TMS pulse was preceded by CPN stimulation with a CT interval of 35 ms, and they were facilitated for CT intervals of 50-55 ms. A similar inhibition of the soleus H-reflex was not observed. To investigate which descending pathways might be responsible for the afferent-evoked inhibition and facilitation, we examined the effect of CPN stimulation on short-latency facilitation (SLF) and long-latency facilitation (LLF) of the soleus H-reflex induced by a subthreshold TMS-pulse at different CT intervals. SLF is known to reflect the excitability of the fastest conducting, corticomotoneuronal, cells whereas LLF is believed to be caused by more indirect descending pathways. At CT intervals of 40-45 ms, the LLF was significantly more inhibited compared to the SLF when taking the effect on the H-reflex into account. Finally, we investigated how the CPN-induced inhibition and facilitation of the soleus MEP were modulated prior to dorsiflexion. Whereas the late facilitation (CT interval: 55 ms) was similar prior to dorsiflexion and at rest, no inhibition could be evoked at the earlier latency (CT interval: 35 ms) prior to onset of dorsiflexion.The observation that the CPN-induced inhibition of soleus MEPs disappears prior to onset of dorsiflexion may explain why soleus MEPs are facilitated prior to onset of dorsiflexion contraction. A possible mechanism involves the removal of inhibition of the descending command to the motoneurons at a spinal interneuronal level because the inhibition was seen in LLF and not in SLF and the MEP-inhibition was not observed in the H-reflex. The data illustrate that spinal interneuronal pathways modify descending commands to human spinal motoneurons and influence the size of MEPs elicited by TMS.

AB - It has recently been demonstrated that soleus motor evoked potentials (MEPs) are facilitated prior to the onset of dorsiflexion. The purpose of this study was to examine if this could be explained by removal of spinal inhibition of the descending command to soleus motoneurons. To test this, we investigated how afferent inputs from the tibialis anterior muscle modulate the corticospinal activation of soleus spinal motoneurons at rest, during static contraction and prior to movement. MEPs activated by transcranial magnetic stimulation (TMS) and Hoffmann-reflexes (H-reflexes) activated by electrical stimulation of the posterior tibial nerve (PTN) were conditioned by prior stimulation of the common peroneal nerve (CPN) at a variety of conditioning-test (CT) intervals.MEPs in the precontracted soleus muscle were inhibited when the TMS pulse was preceded by CPN stimulation with a CT interval of 35 ms, and they were facilitated for CT intervals of 50-55 ms. A similar inhibition of the soleus H-reflex was not observed. To investigate which descending pathways might be responsible for the afferent-evoked inhibition and facilitation, we examined the effect of CPN stimulation on short-latency facilitation (SLF) and long-latency facilitation (LLF) of the soleus H-reflex induced by a subthreshold TMS-pulse at different CT intervals. SLF is known to reflect the excitability of the fastest conducting, corticomotoneuronal, cells whereas LLF is believed to be caused by more indirect descending pathways. At CT intervals of 40-45 ms, the LLF was significantly more inhibited compared to the SLF when taking the effect on the H-reflex into account. Finally, we investigated how the CPN-induced inhibition and facilitation of the soleus MEP were modulated prior to dorsiflexion. Whereas the late facilitation (CT interval: 55 ms) was similar prior to dorsiflexion and at rest, no inhibition could be evoked at the earlier latency (CT interval: 35 ms) prior to onset of dorsiflexion.The observation that the CPN-induced inhibition of soleus MEPs disappears prior to onset of dorsiflexion may explain why soleus MEPs are facilitated prior to onset of dorsiflexion contraction. A possible mechanism involves the removal of inhibition of the descending command to the motoneurons at a spinal interneuronal level because the inhibition was seen in LLF and not in SLF and the MEP-inhibition was not observed in the H-reflex. The data illustrate that spinal interneuronal pathways modify descending commands to human spinal motoneurons and influence the size of MEPs elicited by TMS.

U2 - 10.1113/jphysiol.2011.214387

DO - 10.1113/jphysiol.2011.214387

M3 - Journal article

C2 - 21986208

VL - 589

SP - 5819

EP - 5831

JO - The Journal of Physiology

JF - The Journal of Physiology

SN - 0022-3751

IS - 23

ER -

ID: 35063749