Altered Regulation of Ia Afferent Input during Voluntary Activity after Human Spinal Cord Injury

Abstract Sensory input converging on the spinal cord contributes to the control of voluntary activity. Although sensory pathways reorganize following spinal cord injury (SCI), the extent to which sensory input from Ia afferents is regulated during voluntary activity after the injury remains largely unknown. To address this question, we examined the soleus H-reflex and conditioning of the H-reflex by stimulating homonymous and heteronymous nerves [depression of the soleus H-reflex evoked by common peroneal nerve stimulation (D1 inhibition) and the monosynaptic Ia facilitation of the soleus H-reflex evoked by femoral nerve stimulation (FN facilitation)] at rest, and during tonic voluntary activity in humans with and without chronic incomplete SCI. We found that during voluntary activity the soleus H-reflex size increased in both groups compared with rest, but to a lesser extent in SCI participants. Compared with rest, the D1 inhibition decreased during voluntary activity in controls but it was still present in SCI participants. Further, the FN facilitation increased in controls but remained unchanged in SCI participants during voluntary activity compared with rest. Changes in the D1 inhibition and FN facilitation were correlated with changes in the H-reflex during voluntary activity, suggesting an association between outcomes. These findings provide the first demonstration that the regulation of Ia afferent input from homonymous and heteronymous nerves is altered during voluntary in humans with SCI, resulting in lesser facilitatory effect on motor neurons..

Medienart:

Preprint

Erscheinungsjahr:

2023

Erschienen:

2023

Enthalten in:

bioRxiv.org - (2023) vom: 21. Nov. Zur Gesamtaufnahme - year:2023

Sprache:

Englisch

Beteiligte Personen:

Chen, Bing [VerfasserIn]
Perez, Monica A. [VerfasserIn]

Links:

Volltext [lizenzpflichtig]
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Themen:

570
Biology

doi:

10.1101/2022.05.15.492010

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

XBI036035084