Authors: Timothy J Carroll Evan R L Baldwin David F Collins
Publish Date: 2004/11/13
Volume: 161, Issue: 3, Pages: 299-306
Abstract
To study the regulation of the Renshaw cellmediated inhibitory pathway from ECR to FCR motoneurons forty stimuli were delivered to the radial nerve at 50 of the maximal Mwave amplitude for ECR brevis Stimuli were delivered during both isometric wrist flexions and radial deviation actions with an equivalent EMG amplitude in FCR ~5 wrist flexion MVCTo explore the homonymous Ia afferent pathway to FCR motoneurons 50 stimuli were delivered to the median nerve at intensities ranging from below motor threshold to at least two times that which evoked a maximal Mwave during wrist flexion and radial deviation matched FCR EMG at ~5 wrist flexion MVCThere was no significant difference in the inhibition of FCR EMG induced via ECRcoupled Renshaw cells between radial deviation and wrist flexion However the mean FCR Hreflex amplitude was significantly P005 greater during wrist flexion than radial deviation Furthermore EMG amplitude in FCR and ECR brevis was significantly P005 greater during MVCs in wrist flexion and extension respectively than radial deviation ECR longus EMG was significantly greater during MVCs in radial deviation than extension These results indicate that the gain of the Renshawmediated inhibitory pathway between ECR and FCR motoneurons is similar for weak flexion and radial deviation actions However the gain of the Hreflex pathway to FCR is greater during wrist flexion than radial deviation Transmission through both of these pathways probably contributes to the inability of individuals to maximally activate FCR during radial deviation MVCs
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