Task dependent gain regulation of spinal circuits projecting to the human flexor carpi radialis
Abstract In humans, the flexor carpi radialis (FCR) and extensor carpi radialis (ECR) muscles act as antagonists during wrist flexion-extension and as functional synergists during radial deviation. In contrast to the situation in most antagonist muscle pairs, Renshaw cells innervated by the motor ne...
Ausführliche Beschreibung
Autor*in: |
Carroll, Timothy J. [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2004 |
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Anmerkung: |
© Springer-Verlag 2004 |
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Übergeordnetes Werk: |
Enthalten in: Experimental brain research - Berlin : Springer, 1966, 161(2004), 3 vom: 13. Nov., Seite 299-306 |
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Übergeordnetes Werk: |
volume:161 ; year:2004 ; number:3 ; day:13 ; month:11 ; pages:299-306 |
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DOI / URN: |
10.1007/s00221-004-2072-1 |
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Katalog-ID: |
SPR002385783 |
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520 | |a Abstract In humans, the flexor carpi radialis (FCR) and extensor carpi radialis (ECR) muscles act as antagonists during wrist flexion-extension and as functional synergists during radial deviation. In contrast to the situation in most antagonist muscle pairs, Renshaw cells innervated by the motor neurons of each muscle inhibit the motoneurons, but not Ia inhibitory interneurons, of the opposite motor pool. Here we compared gain regulation of spinal circuits projecting to FCR motoneurons during two tasks: flexion and radial deviation of the wrist. We also investigated the functional consequences of this organisation for maximal voluntary contractions (MVCs). Electromyographic (EMG) recordings were taken from FCR, ECR longus and ECR brevis using fine-wire electrodes and electrical stimulation was delivered to the median and radial nerves. Ten volunteers participated in three experiments.To study the regulation of the Renshaw cell-mediated, inhibitory pathway from ECR to FCR motoneurons, forty stimuli were delivered to the radial nerve at 50% of the maximal M-wave 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 MVC).To 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 M-wave during wrist flexion and radial deviation (matched FCR EMG at ~5% wrist flexion MVC).EMG amplitude was measured during MVCs in wrist flexion, extension and radial deviation. There was no significant difference in the inhibition of FCR EMG induced via ECR-coupled Renshaw cells between radial deviation and wrist flexion. However, the mean FCR H-reflex amplitude was significantly (P<0.05) greater during wrist flexion than radial deviation. Furthermore, EMG amplitude in FCR and ECR brevis was significantly (P<0.05) 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 Renshaw-mediated inhibitory pathway between ECR and FCR motoneurons is similar for weak flexion and radial deviation actions. However, the gain of the H-reflex 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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650 | 4 | |a FCR |7 (dpeaa)DE-He213 | |
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700 | 1 | |a Baldwin, Evan R. L. |4 aut | |
700 | 1 | |a Collins, David F. |4 aut | |
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10.1007/s00221-004-2072-1 doi (DE-627)SPR002385783 (SPR)s00221-004-2072-1-e DE-627 ger DE-627 rakwb eng Carroll, Timothy J. verfasserin aut Task dependent gain regulation of spinal circuits projecting to the human flexor carpi radialis 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2004 Abstract In humans, the flexor carpi radialis (FCR) and extensor carpi radialis (ECR) muscles act as antagonists during wrist flexion-extension and as functional synergists during radial deviation. In contrast to the situation in most antagonist muscle pairs, Renshaw cells innervated by the motor neurons of each muscle inhibit the motoneurons, but not Ia inhibitory interneurons, of the opposite motor pool. Here we compared gain regulation of spinal circuits projecting to FCR motoneurons during two tasks: flexion and radial deviation of the wrist. We also investigated the functional consequences of this organisation for maximal voluntary contractions (MVCs). Electromyographic (EMG) recordings were taken from FCR, ECR longus and ECR brevis using fine-wire electrodes and electrical stimulation was delivered to the median and radial nerves. Ten volunteers participated in three experiments.To study the regulation of the Renshaw cell-mediated, inhibitory pathway from ECR to FCR motoneurons, forty stimuli were delivered to the radial nerve at 50% of the maximal M-wave 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 MVC).To 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 M-wave during wrist flexion and radial deviation (matched FCR EMG at ~5% wrist flexion MVC).EMG amplitude was measured during MVCs in wrist flexion, extension and radial deviation. There was no significant difference in the inhibition of FCR EMG induced via ECR-coupled Renshaw cells between radial deviation and wrist flexion. However, the mean FCR H-reflex amplitude was significantly (P<0.05) greater during wrist flexion than radial deviation. Furthermore, EMG amplitude in FCR and ECR brevis was significantly (P<0.05) 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 Renshaw-mediated inhibitory pathway between ECR and FCR motoneurons is similar for weak flexion and radial deviation actions. However, the gain of the H-reflex 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. H-reflex (dpeaa)DE-He213 FCR (dpeaa)DE-He213 ECR (dpeaa)DE-He213 Renshaw cell (dpeaa)DE-He213 Wrist muscle (dpeaa)DE-He213 Co-contraction (dpeaa)DE-He213 Maximum voluntary contraction (dpeaa)DE-He213 Baldwin, Evan R. L. aut Collins, David F. aut Enthalten in Experimental brain research Berlin : Springer, 1966 161(2004), 3 vom: 13. Nov., Seite 299-306 (DE-627)253723159 (DE-600)1459099-2 1432-1106 nnns volume:161 year:2004 number:3 day:13 month:11 pages:299-306 https://dx.doi.org/10.1007/s00221-004-2072-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 161 2004 3 13 11 299-306 |
spelling |
10.1007/s00221-004-2072-1 doi (DE-627)SPR002385783 (SPR)s00221-004-2072-1-e DE-627 ger DE-627 rakwb eng Carroll, Timothy J. verfasserin aut Task dependent gain regulation of spinal circuits projecting to the human flexor carpi radialis 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2004 Abstract In humans, the flexor carpi radialis (FCR) and extensor carpi radialis (ECR) muscles act as antagonists during wrist flexion-extension and as functional synergists during radial deviation. In contrast to the situation in most antagonist muscle pairs, Renshaw cells innervated by the motor neurons of each muscle inhibit the motoneurons, but not Ia inhibitory interneurons, of the opposite motor pool. Here we compared gain regulation of spinal circuits projecting to FCR motoneurons during two tasks: flexion and radial deviation of the wrist. We also investigated the functional consequences of this organisation for maximal voluntary contractions (MVCs). Electromyographic (EMG) recordings were taken from FCR, ECR longus and ECR brevis using fine-wire electrodes and electrical stimulation was delivered to the median and radial nerves. Ten volunteers participated in three experiments.To study the regulation of the Renshaw cell-mediated, inhibitory pathway from ECR to FCR motoneurons, forty stimuli were delivered to the radial nerve at 50% of the maximal M-wave 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 MVC).To 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 M-wave during wrist flexion and radial deviation (matched FCR EMG at ~5% wrist flexion MVC).EMG amplitude was measured during MVCs in wrist flexion, extension and radial deviation. There was no significant difference in the inhibition of FCR EMG induced via ECR-coupled Renshaw cells between radial deviation and wrist flexion. However, the mean FCR H-reflex amplitude was significantly (P<0.05) greater during wrist flexion than radial deviation. Furthermore, EMG amplitude in FCR and ECR brevis was significantly (P<0.05) 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 Renshaw-mediated inhibitory pathway between ECR and FCR motoneurons is similar for weak flexion and radial deviation actions. However, the gain of the H-reflex 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. H-reflex (dpeaa)DE-He213 FCR (dpeaa)DE-He213 ECR (dpeaa)DE-He213 Renshaw cell (dpeaa)DE-He213 Wrist muscle (dpeaa)DE-He213 Co-contraction (dpeaa)DE-He213 Maximum voluntary contraction (dpeaa)DE-He213 Baldwin, Evan R. L. aut Collins, David F. aut Enthalten in Experimental brain research Berlin : Springer, 1966 161(2004), 3 vom: 13. Nov., Seite 299-306 (DE-627)253723159 (DE-600)1459099-2 1432-1106 nnns volume:161 year:2004 number:3 day:13 month:11 pages:299-306 https://dx.doi.org/10.1007/s00221-004-2072-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 161 2004 3 13 11 299-306 |
allfields_unstemmed |
10.1007/s00221-004-2072-1 doi (DE-627)SPR002385783 (SPR)s00221-004-2072-1-e DE-627 ger DE-627 rakwb eng Carroll, Timothy J. verfasserin aut Task dependent gain regulation of spinal circuits projecting to the human flexor carpi radialis 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2004 Abstract In humans, the flexor carpi radialis (FCR) and extensor carpi radialis (ECR) muscles act as antagonists during wrist flexion-extension and as functional synergists during radial deviation. In contrast to the situation in most antagonist muscle pairs, Renshaw cells innervated by the motor neurons of each muscle inhibit the motoneurons, but not Ia inhibitory interneurons, of the opposite motor pool. Here we compared gain regulation of spinal circuits projecting to FCR motoneurons during two tasks: flexion and radial deviation of the wrist. We also investigated the functional consequences of this organisation for maximal voluntary contractions (MVCs). Electromyographic (EMG) recordings were taken from FCR, ECR longus and ECR brevis using fine-wire electrodes and electrical stimulation was delivered to the median and radial nerves. Ten volunteers participated in three experiments.To study the regulation of the Renshaw cell-mediated, inhibitory pathway from ECR to FCR motoneurons, forty stimuli were delivered to the radial nerve at 50% of the maximal M-wave 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 MVC).To 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 M-wave during wrist flexion and radial deviation (matched FCR EMG at ~5% wrist flexion MVC).EMG amplitude was measured during MVCs in wrist flexion, extension and radial deviation. There was no significant difference in the inhibition of FCR EMG induced via ECR-coupled Renshaw cells between radial deviation and wrist flexion. However, the mean FCR H-reflex amplitude was significantly (P<0.05) greater during wrist flexion than radial deviation. Furthermore, EMG amplitude in FCR and ECR brevis was significantly (P<0.05) 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 Renshaw-mediated inhibitory pathway between ECR and FCR motoneurons is similar for weak flexion and radial deviation actions. However, the gain of the H-reflex 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. H-reflex (dpeaa)DE-He213 FCR (dpeaa)DE-He213 ECR (dpeaa)DE-He213 Renshaw cell (dpeaa)DE-He213 Wrist muscle (dpeaa)DE-He213 Co-contraction (dpeaa)DE-He213 Maximum voluntary contraction (dpeaa)DE-He213 Baldwin, Evan R. L. aut Collins, David F. aut Enthalten in Experimental brain research Berlin : Springer, 1966 161(2004), 3 vom: 13. Nov., Seite 299-306 (DE-627)253723159 (DE-600)1459099-2 1432-1106 nnns volume:161 year:2004 number:3 day:13 month:11 pages:299-306 https://dx.doi.org/10.1007/s00221-004-2072-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 161 2004 3 13 11 299-306 |
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10.1007/s00221-004-2072-1 doi (DE-627)SPR002385783 (SPR)s00221-004-2072-1-e DE-627 ger DE-627 rakwb eng Carroll, Timothy J. verfasserin aut Task dependent gain regulation of spinal circuits projecting to the human flexor carpi radialis 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2004 Abstract In humans, the flexor carpi radialis (FCR) and extensor carpi radialis (ECR) muscles act as antagonists during wrist flexion-extension and as functional synergists during radial deviation. In contrast to the situation in most antagonist muscle pairs, Renshaw cells innervated by the motor neurons of each muscle inhibit the motoneurons, but not Ia inhibitory interneurons, of the opposite motor pool. Here we compared gain regulation of spinal circuits projecting to FCR motoneurons during two tasks: flexion and radial deviation of the wrist. We also investigated the functional consequences of this organisation for maximal voluntary contractions (MVCs). Electromyographic (EMG) recordings were taken from FCR, ECR longus and ECR brevis using fine-wire electrodes and electrical stimulation was delivered to the median and radial nerves. Ten volunteers participated in three experiments.To study the regulation of the Renshaw cell-mediated, inhibitory pathway from ECR to FCR motoneurons, forty stimuli were delivered to the radial nerve at 50% of the maximal M-wave 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 MVC).To 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 M-wave during wrist flexion and radial deviation (matched FCR EMG at ~5% wrist flexion MVC).EMG amplitude was measured during MVCs in wrist flexion, extension and radial deviation. There was no significant difference in the inhibition of FCR EMG induced via ECR-coupled Renshaw cells between radial deviation and wrist flexion. However, the mean FCR H-reflex amplitude was significantly (P<0.05) greater during wrist flexion than radial deviation. Furthermore, EMG amplitude in FCR and ECR brevis was significantly (P<0.05) 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 Renshaw-mediated inhibitory pathway between ECR and FCR motoneurons is similar for weak flexion and radial deviation actions. However, the gain of the H-reflex 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. H-reflex (dpeaa)DE-He213 FCR (dpeaa)DE-He213 ECR (dpeaa)DE-He213 Renshaw cell (dpeaa)DE-He213 Wrist muscle (dpeaa)DE-He213 Co-contraction (dpeaa)DE-He213 Maximum voluntary contraction (dpeaa)DE-He213 Baldwin, Evan R. L. aut Collins, David F. aut Enthalten in Experimental brain research Berlin : Springer, 1966 161(2004), 3 vom: 13. Nov., Seite 299-306 (DE-627)253723159 (DE-600)1459099-2 1432-1106 nnns volume:161 year:2004 number:3 day:13 month:11 pages:299-306 https://dx.doi.org/10.1007/s00221-004-2072-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 161 2004 3 13 11 299-306 |
allfieldsSound |
10.1007/s00221-004-2072-1 doi (DE-627)SPR002385783 (SPR)s00221-004-2072-1-e DE-627 ger DE-627 rakwb eng Carroll, Timothy J. verfasserin aut Task dependent gain regulation of spinal circuits projecting to the human flexor carpi radialis 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2004 Abstract In humans, the flexor carpi radialis (FCR) and extensor carpi radialis (ECR) muscles act as antagonists during wrist flexion-extension and as functional synergists during radial deviation. In contrast to the situation in most antagonist muscle pairs, Renshaw cells innervated by the motor neurons of each muscle inhibit the motoneurons, but not Ia inhibitory interneurons, of the opposite motor pool. Here we compared gain regulation of spinal circuits projecting to FCR motoneurons during two tasks: flexion and radial deviation of the wrist. We also investigated the functional consequences of this organisation for maximal voluntary contractions (MVCs). Electromyographic (EMG) recordings were taken from FCR, ECR longus and ECR brevis using fine-wire electrodes and electrical stimulation was delivered to the median and radial nerves. Ten volunteers participated in three experiments.To study the regulation of the Renshaw cell-mediated, inhibitory pathway from ECR to FCR motoneurons, forty stimuli were delivered to the radial nerve at 50% of the maximal M-wave 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 MVC).To 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 M-wave during wrist flexion and radial deviation (matched FCR EMG at ~5% wrist flexion MVC).EMG amplitude was measured during MVCs in wrist flexion, extension and radial deviation. There was no significant difference in the inhibition of FCR EMG induced via ECR-coupled Renshaw cells between radial deviation and wrist flexion. However, the mean FCR H-reflex amplitude was significantly (P<0.05) greater during wrist flexion than radial deviation. Furthermore, EMG amplitude in FCR and ECR brevis was significantly (P<0.05) 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 Renshaw-mediated inhibitory pathway between ECR and FCR motoneurons is similar for weak flexion and radial deviation actions. However, the gain of the H-reflex 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. H-reflex (dpeaa)DE-He213 FCR (dpeaa)DE-He213 ECR (dpeaa)DE-He213 Renshaw cell (dpeaa)DE-He213 Wrist muscle (dpeaa)DE-He213 Co-contraction (dpeaa)DE-He213 Maximum voluntary contraction (dpeaa)DE-He213 Baldwin, Evan R. L. aut Collins, David F. aut Enthalten in Experimental brain research Berlin : Springer, 1966 161(2004), 3 vom: 13. Nov., Seite 299-306 (DE-627)253723159 (DE-600)1459099-2 1432-1106 nnns volume:161 year:2004 number:3 day:13 month:11 pages:299-306 https://dx.doi.org/10.1007/s00221-004-2072-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 161 2004 3 13 11 299-306 |
language |
English |
source |
Enthalten in Experimental brain research 161(2004), 3 vom: 13. Nov., Seite 299-306 volume:161 year:2004 number:3 day:13 month:11 pages:299-306 |
sourceStr |
Enthalten in Experimental brain research 161(2004), 3 vom: 13. Nov., Seite 299-306 volume:161 year:2004 number:3 day:13 month:11 pages:299-306 |
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Experimental brain research |
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Carroll, Timothy J. @@aut@@ Baldwin, Evan R. L. @@aut@@ Collins, David F. @@aut@@ |
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Carroll, Timothy J. |
spellingShingle |
Carroll, Timothy J. misc H-reflex misc FCR misc ECR misc Renshaw cell misc Wrist muscle misc Co-contraction misc Maximum voluntary contraction Task dependent gain regulation of spinal circuits projecting to the human flexor carpi radialis |
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Task dependent gain regulation of spinal circuits projecting to the human flexor carpi radialis H-reflex (dpeaa)DE-He213 FCR (dpeaa)DE-He213 ECR (dpeaa)DE-He213 Renshaw cell (dpeaa)DE-He213 Wrist muscle (dpeaa)DE-He213 Co-contraction (dpeaa)DE-He213 Maximum voluntary contraction (dpeaa)DE-He213 |
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misc H-reflex misc FCR misc ECR misc Renshaw cell misc Wrist muscle misc Co-contraction misc Maximum voluntary contraction |
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Task dependent gain regulation of spinal circuits projecting to the human flexor carpi radialis |
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Task dependent gain regulation of spinal circuits projecting to the human flexor carpi radialis |
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Experimental brain research |
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Carroll, Timothy J. Baldwin, Evan R. L. Collins, David F. |
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10.1007/s00221-004-2072-1 |
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task dependent gain regulation of spinal circuits projecting to the human flexor carpi radialis |
title_auth |
Task dependent gain regulation of spinal circuits projecting to the human flexor carpi radialis |
abstract |
Abstract In humans, the flexor carpi radialis (FCR) and extensor carpi radialis (ECR) muscles act as antagonists during wrist flexion-extension and as functional synergists during radial deviation. In contrast to the situation in most antagonist muscle pairs, Renshaw cells innervated by the motor neurons of each muscle inhibit the motoneurons, but not Ia inhibitory interneurons, of the opposite motor pool. Here we compared gain regulation of spinal circuits projecting to FCR motoneurons during two tasks: flexion and radial deviation of the wrist. We also investigated the functional consequences of this organisation for maximal voluntary contractions (MVCs). Electromyographic (EMG) recordings were taken from FCR, ECR longus and ECR brevis using fine-wire electrodes and electrical stimulation was delivered to the median and radial nerves. Ten volunteers participated in three experiments.To study the regulation of the Renshaw cell-mediated, inhibitory pathway from ECR to FCR motoneurons, forty stimuli were delivered to the radial nerve at 50% of the maximal M-wave 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 MVC).To 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 M-wave during wrist flexion and radial deviation (matched FCR EMG at ~5% wrist flexion MVC).EMG amplitude was measured during MVCs in wrist flexion, extension and radial deviation. There was no significant difference in the inhibition of FCR EMG induced via ECR-coupled Renshaw cells between radial deviation and wrist flexion. However, the mean FCR H-reflex amplitude was significantly (P<0.05) greater during wrist flexion than radial deviation. Furthermore, EMG amplitude in FCR and ECR brevis was significantly (P<0.05) 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 Renshaw-mediated inhibitory pathway between ECR and FCR motoneurons is similar for weak flexion and radial deviation actions. However, the gain of the H-reflex 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. © Springer-Verlag 2004 |
abstractGer |
Abstract In humans, the flexor carpi radialis (FCR) and extensor carpi radialis (ECR) muscles act as antagonists during wrist flexion-extension and as functional synergists during radial deviation. In contrast to the situation in most antagonist muscle pairs, Renshaw cells innervated by the motor neurons of each muscle inhibit the motoneurons, but not Ia inhibitory interneurons, of the opposite motor pool. Here we compared gain regulation of spinal circuits projecting to FCR motoneurons during two tasks: flexion and radial deviation of the wrist. We also investigated the functional consequences of this organisation for maximal voluntary contractions (MVCs). Electromyographic (EMG) recordings were taken from FCR, ECR longus and ECR brevis using fine-wire electrodes and electrical stimulation was delivered to the median and radial nerves. Ten volunteers participated in three experiments.To study the regulation of the Renshaw cell-mediated, inhibitory pathway from ECR to FCR motoneurons, forty stimuli were delivered to the radial nerve at 50% of the maximal M-wave 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 MVC).To 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 M-wave during wrist flexion and radial deviation (matched FCR EMG at ~5% wrist flexion MVC).EMG amplitude was measured during MVCs in wrist flexion, extension and radial deviation. There was no significant difference in the inhibition of FCR EMG induced via ECR-coupled Renshaw cells between radial deviation and wrist flexion. However, the mean FCR H-reflex amplitude was significantly (P<0.05) greater during wrist flexion than radial deviation. Furthermore, EMG amplitude in FCR and ECR brevis was significantly (P<0.05) 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 Renshaw-mediated inhibitory pathway between ECR and FCR motoneurons is similar for weak flexion and radial deviation actions. However, the gain of the H-reflex 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. © Springer-Verlag 2004 |
abstract_unstemmed |
Abstract In humans, the flexor carpi radialis (FCR) and extensor carpi radialis (ECR) muscles act as antagonists during wrist flexion-extension and as functional synergists during radial deviation. In contrast to the situation in most antagonist muscle pairs, Renshaw cells innervated by the motor neurons of each muscle inhibit the motoneurons, but not Ia inhibitory interneurons, of the opposite motor pool. Here we compared gain regulation of spinal circuits projecting to FCR motoneurons during two tasks: flexion and radial deviation of the wrist. We also investigated the functional consequences of this organisation for maximal voluntary contractions (MVCs). Electromyographic (EMG) recordings were taken from FCR, ECR longus and ECR brevis using fine-wire electrodes and electrical stimulation was delivered to the median and radial nerves. Ten volunteers participated in three experiments.To study the regulation of the Renshaw cell-mediated, inhibitory pathway from ECR to FCR motoneurons, forty stimuli were delivered to the radial nerve at 50% of the maximal M-wave 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 MVC).To 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 M-wave during wrist flexion and radial deviation (matched FCR EMG at ~5% wrist flexion MVC).EMG amplitude was measured during MVCs in wrist flexion, extension and radial deviation. There was no significant difference in the inhibition of FCR EMG induced via ECR-coupled Renshaw cells between radial deviation and wrist flexion. However, the mean FCR H-reflex amplitude was significantly (P<0.05) greater during wrist flexion than radial deviation. Furthermore, EMG amplitude in FCR and ECR brevis was significantly (P<0.05) 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 Renshaw-mediated inhibitory pathway between ECR and FCR motoneurons is similar for weak flexion and radial deviation actions. However, the gain of the H-reflex 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. © Springer-Verlag 2004 |
collection_details |
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container_issue |
3 |
title_short |
Task dependent gain regulation of spinal circuits projecting to the human flexor carpi radialis |
url |
https://dx.doi.org/10.1007/s00221-004-2072-1 |
remote_bool |
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author2 |
Baldwin, Evan R. L. Collins, David F. |
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Baldwin, Evan R. L. Collins, David F. |
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doi_str |
10.1007/s00221-004-2072-1 |
up_date |
2024-07-04T02:49:17.744Z |
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|
score |
7.401515 |