Neural mechanisms involved in the functional linking of motor cortical points
Neural mechanisms involved in the functional linking of motor cortical points
We sought to understand the basic neural processes involved in the functional linking of motor cortical points. We asked which of the two basic neural mechanisms, excitation or inhibition, is required to functionally link motor cortical points. In the ketamine-anaesthetized cat, a microstimulation electrode was positioned at a point (control point) that was identified by the following three characteristics of the EMG responses: the muscle(s) activated at threshold, any additional muscles recruited by supra-threshold stimulation, and their relative latency. A second distinct point (test point) producing activation of a muscle at a different joint was then identified. At this test cortical point the GABAA receptor antagonist bicuculline was ejected iontophoretically, while stimulating the control point near threshold. A combined response was elicited consisting of the response normally elicited at the control point plus that elicited at the test point. Thus, an artificial muscle synergy was produced following disinhibition of the test point. This was never the case when glutamate was ejected at the test point, even when supra-threshold stimuli were used at the control point. Therefore, simply increasing the excitability of a cortical point was not sufficient to release the muscle(s) represented at that point into a muscle synergy. Kynurenate, a broadly acting excitatory amino acid receptor antagonist, ejected at the bicuculline point reversed the effect of bicuculline. This shows that the release phenomenon was mediated synaptically and was not due to spread of the stimulating current. We suggest that release from inhibition may be one of the neural mechanisms involved in functionally linking motor cortical points. This functional linking may be part of the ensemble of motor cortical mechanisms involved in recruitment of muscle synergies.
disinhibition, intracortical inhibition, bicuculline, motor synergies, multi-joint movements, motor cortex, GABAergic inhibition
86-94
Schneider, Cyril
fe903f40-11d5-454d-9d17-514bbc717864
Devanne, Hervé
00e7dabb-8640-449e-8662-0d4c663ce1da
Lavoie, Brigitte A.
8acd6a26-0768-41c6-874b-27c226764692
Capaday, Charles
0f389225-5082-4b7d-bc4d-cb35e90385a5
2002
Schneider, Cyril
fe903f40-11d5-454d-9d17-514bbc717864
Devanne, Hervé
00e7dabb-8640-449e-8662-0d4c663ce1da
Lavoie, Brigitte A.
8acd6a26-0768-41c6-874b-27c226764692
Capaday, Charles
0f389225-5082-4b7d-bc4d-cb35e90385a5
Schneider, Cyril, Devanne, Hervé, Lavoie, Brigitte A. and Capaday, Charles
(2002)
Neural mechanisms involved in the functional linking of motor cortical points.
Experimental Brain Research, 146 (1), .
(doi:10.1007/s00221-002-1137-2).
Abstract
We sought to understand the basic neural processes involved in the functional linking of motor cortical points. We asked which of the two basic neural mechanisms, excitation or inhibition, is required to functionally link motor cortical points. In the ketamine-anaesthetized cat, a microstimulation electrode was positioned at a point (control point) that was identified by the following three characteristics of the EMG responses: the muscle(s) activated at threshold, any additional muscles recruited by supra-threshold stimulation, and their relative latency. A second distinct point (test point) producing activation of a muscle at a different joint was then identified. At this test cortical point the GABAA receptor antagonist bicuculline was ejected iontophoretically, while stimulating the control point near threshold. A combined response was elicited consisting of the response normally elicited at the control point plus that elicited at the test point. Thus, an artificial muscle synergy was produced following disinhibition of the test point. This was never the case when glutamate was ejected at the test point, even when supra-threshold stimuli were used at the control point. Therefore, simply increasing the excitability of a cortical point was not sufficient to release the muscle(s) represented at that point into a muscle synergy. Kynurenate, a broadly acting excitatory amino acid receptor antagonist, ejected at the bicuculline point reversed the effect of bicuculline. This shows that the release phenomenon was mediated synaptically and was not due to spread of the stimulating current. We suggest that release from inhibition may be one of the neural mechanisms involved in functionally linking motor cortical points. This functional linking may be part of the ensemble of motor cortical mechanisms involved in recruitment of muscle synergies.
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Published date: 2002
Keywords:
disinhibition, intracortical inhibition, bicuculline, motor synergies, multi-joint movements, motor cortex, GABAergic inhibition
Identifiers
Local EPrints ID: 27708
URI: http://eprints.soton.ac.uk/id/eprint/27708
ISSN: 0014-4819
PURE UUID: 7e884664-cbee-4329-9c3a-7e081bc58c3b
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Date deposited: 25 Apr 2006
Last modified: 15 Mar 2024 07:20
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Contributors
Author:
Cyril Schneider
Author:
Hervé Devanne
Author:
Brigitte A. Lavoie
Author:
Charles Capaday
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