Electrocorticographic activity over sensorimotor cortex and motor function in awake behaving rats.

TitleElectrocorticographic activity over sensorimotor cortex and motor function in awake behaving rats.
Publication TypeJournal Article
Year of Publication2015
AuthorsBoulay, CB, Chen, XY, Wolpaw, J
JournalJ Neurophysiol
Volume113
Issue7
Pagination2232-41
Date Published04/2015
ISSN1522-1598
Keywordsbrain-computer interface, cortex, H-Reflex, Motor control, Spinal Cord
Abstract

Sensorimotor cortex exerts both short-term and long-term control over the spinal reflex pathways that serve motor behaviors. Better understanding of this control could offer new possibilities for restoring function after central nervous system trauma or disease. We examined the impact of ongoing sensorimotor cortex (SMC) activity on the largely monosynaptic pathway of the H-reflex, the electrical analog of the spinal stretch reflex. In 41 awake adult rats, we measured soleus electromyographic (EMG) activity, the soleus H-reflex, and electrocorticographic activity over the contralateral SMC while rats were producing steady-state soleus EMG activity. Principal component analysis of electrocorticographic frequency spectra before H-reflex elicitation consistently revealed three frequency bands: μβ (5-30 Hz), low γ (γ1; 40-85 Hz), and high γ (γ2; 100-200 Hz). Ongoing (i.e., background) soleus EMG amplitude correlated negatively with μβ power and positively with γ1 power. In contrast, H-reflex size correlated positively with μβ power and negatively with γ1 power, but only when background soleus EMG amplitude was included in the linear model. These results support the hypothesis that increased SMC activation (indicated by decrease in μβ power and/or increase in γ1 power) simultaneously potentiates the H-reflex by exciting spinal motoneurons and suppresses it by decreasing the efficacy of the afferent input. They may help guide the development of new rehabilitation methods and of brain-computer interfaces that use SMC activity as a substitute for lost or impaired motor outputs.

URLhttp://www.ncbi.nlm.nih.gov/pubmed/25632076
DOI10.1152/jn.00677.2014
Alternate JournalJ. Neurophysiol.
PubMed ID25632076
PubMed Central IDPMC4416631
Grant ListP41 EB018783 / EB / NIBIB NIH HHS / United States
R01 EB000856 / EB / NIBIB NIH HHS / United States

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