scholarly journals Developmental 'awakening' of primary motor cortex to the sensory consequences of movement

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
James C Dooley ◽  
Mark S Blumberg
Keyword(s):  
Motor Control ◽  
Motor Cortex ◽  
Somatosensory Cortex ◽  
Primary Motor Cortex ◽  
Cuneate Nucleus ◽  
Somatosensory Area ◽  
External Cuneate Nucleus ◽  
Full Complement ◽  
Sensory Responses ◽  
Rapid Shift

Before primary motor cortex (M1) develops its motor functions, it functions like a somatosensory area. Here, by recording from neurons in the forelimb representation of M1 in postnatal day (P) 8–12 rats, we demonstrate a rapid shift in its sensory responses. At P8-10, M1 neurons respond overwhelmingly to feedback from sleep-related twitches of the forelimb, but the same neurons do not respond to wake-related movements. By P12, M1 neurons suddenly respond to wake movements, a transition that results from opening the sensory gate in the external cuneate nucleus. Also at P12, fewer M1 neurons respond to individual twitches, but the full complement of twitch-related feedback observed at P8 is unmasked through local disinhibition. Finally, through P12, M1 sensory responses originate in the deep thalamorecipient layers, not primary somatosensory cortex. These findings demonstrate that M1 initially establishes a sensory framework upon which its later-emerging role in motor control is built.

scholarly journals Developmental “awakening” of primary motor cortex to the sensory consequences of movement

2018 ◽  
Author(s):  
James C. Dooley ◽  
Mark S. Blumberg
Keyword(s):  
Motor Control ◽  
Motor Cortex ◽  
Somatosensory Cortex ◽  
Primary Motor Cortex ◽  
Cuneate Nucleus ◽  
Somatosensory Area ◽  
External Cuneate Nucleus ◽  
Full Complement ◽  
Sensory Responses ◽  
Rapid Shift

ABSTRACTBefore primary motor cortex (M1) develops its motor functions, it functions like a somatosensory area. Here, by recording from neurons in the forelimb representation of M1 in postnatal day (P) 8-12 rats, we demonstrate a rapid shift in its sensory responses. At P8-10, M1 neurons respond overwhelmingly to feedback from sleep-related twitches of the forelimb, but the same neurons do not respond to wake-related movements. By P12, M1 neurons suddenly respond to wake movements, a transition that results from opening the sensory gate in the external cuneate nucleus. Also at P12, few M1 neurons respond to twitches, but the full complement of twitch-related feedback observed at P8 can be unmasked through local disinhibition. Finally, through P12, M1 sensory responses originate in the deep thalamorecipient layers, not primary somatosensory cortex. These findings demonstrate that M1 initially establishes a sensory framework upon which its later-emerging role in motor control is built.

Long range high-gamma (60-90 Hz) coupling between primary motor cortex and SMA during motor control revealed by MEG source imaging

NeuroImage ◽  
2009 ◽  
Vol 47 ◽  
pp. S173
Author(s):  
K Jerbi ◽  
H Hui ◽  
D Pantazis ◽  
J-P Lachaux ◽  
O Bertrand ◽  
...  
Keyword(s):  
Motor Control ◽  
Motor Cortex ◽  
Long Range ◽  
Primary Motor Cortex ◽  
Source Imaging ◽  
High Gamma

Sensory responses in motor cortex neurons during precise motor control

1977 ◽  
Vol 5 (5) ◽  
pp. 267-272 ◽  
Author(s):  
Edward V. Evarts ◽  
Christoph Fromm
Keyword(s):  
Motor Control ◽  
Motor Cortex ◽  
Sensory Responses

Motor control: spinal and cortical mechanisms

2016 ◽  
Author(s):  
David Burke
Keyword(s):  
Motor Control ◽  
Motor Cortex ◽  
Voluntary Movement ◽  
Primary Motor Cortex ◽  
Lower Limbs ◽  
Spinal Reflex ◽  
Extensive Literature ◽  
Spinal Level ◽  
Corticospinal System ◽  
The Brain

There is extensive machinery at cerebral and spinal levels to support voluntary movement, but spinal mechanisms are often ignored by clinicians and researchers. For movements of the upper and lower limbs, what the brain commands can be modified or even suppressed completely at spinal level. The corticospinal system is the executive pathway for movement arising largely from primary motor cortex, but movement is not initiated there, and other pathways normally contribute to movement. Greater use of these pathways can allow movement to be restored when the corticospinal system is damaged by, e.g. stroke, but there can be unwanted consequences of this ‘plasticity’. There is an extensive literature on cerebral mechanisms in the control of movement, and an equally large literature on spinal reflex function and the changes that occur during movement, and when pathology results in weakness and/or spasticity.

Functional Properties of Human Primary Motor Cortex Gamma Oscillations

2010 ◽  
Vol 104 (5) ◽  
pp. 2873-2885 ◽  
Author(s):  
Suresh D. Muthukumaraswamy
Keyword(s):  
Motor Control ◽  
Motor Cortex ◽  
Primary Motor Cortex ◽  
Gamma Oscillations ◽  
Finger Movement ◽  
Sensorimotor System ◽  
Repetitive Movement ◽  
Somatosensory Feedback ◽  
Muscle Shortening ◽  
Kinematic Properties

Gamma oscillations in human primary motor cortex (M1) have been described in human electrocorticographic and noninvasive magnetoencephalographic (MEG)/electroencephalographic recordings, yet their functional significance within the sensorimotor system remains unknown. In a set of four MEG experiments described here a number of properties of these oscillations are elucidated. First, gamma oscillations were reliably localized by MEG in M1 and reached peak amplitude 137 ms after electromyographic onset and were not affected by whether movements were cued or self-paced. Gamma oscillations were found to be stronger for larger movements but were absent during the sustained part of isometric movements, with no finger movement or muscle shortening. During repetitive movement sequences gamma oscillations were greater for the first movement of a sequence. Finally, gamma oscillations were absent during passive shortening of the finger compared with active contractions sharing similar kinematic properties demonstrating that M1 oscillations are not simply related to somatosensory feedback. This combined pattern of results is consistent with gamma oscillations playing a role in a relatively late stage of motor control, encoding information related to limb movement rather than to muscle contraction.

Redundant information encoding in primary motor cortex during natural and prosthetic motor control

2011 ◽  
Vol 32 (3) ◽  
pp. 555-561 ◽  
Author(s):  
Kelvin So ◽  
Karunesh Ganguly ◽  
Jessica Jimenez ◽  
Michael C. Gastpar ◽  
Jose M. Carmena
Keyword(s):  
Motor Control ◽  
Motor Cortex ◽  
Primary Motor Cortex ◽  
Redundant Information ◽  
Information Encoding

scholarly journals Layer-specific sensory processing impairment in the primary somatosensory cortex after motor cortex infarction

2019 ◽  
Author(s):  
Atsushi Fukui ◽  
Hironobu Osaki ◽  
Yoshifumi Ueta ◽  
Yoshihiro Muragaki ◽  
Takakazu Kawamata ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Somatosensory Cortex ◽  
Acute Phase ◽  
Sensory Processing ◽  
Primary Motor Cortex ◽  
Temporal Coding ◽  
Network Activity ◽  
Primary Somatosensory Cortex ◽  
Inhibitory Input ◽  
Sensory Impairment

AbstractPrimary motor cortex (M1) infarction occasionally causes sensory impairment. Because sensory signal plays an important role in motor control, sensory impairment compromises recovery and rehabilitation from motor disability. Despite the importance of sensory-motor integration for rehabilitation after M1 infarction, the neural mechanism of the sensory impairment is poorly understood. We show that the sensory processing in the primary somatosensory cortex (S1) was impaired in the acute phase of M1 infarction and recovered in a layer-specific manner in the subacute phase. This layer dependent recovery process and the anatomical connection pattern from M1 to S1 suggested the functional connectivity from M1 to S1 plays a key role in the impairment of sensory processing in S1. The simulation study demonstrated that the loss of inhibition from M1 to S1 in the acute phase of M1 infarction could cause the sensory processing impairment in S1, and the complementation of inhibition could recover the temporal coding. Taken together, we revealed how focal stroke of M1 alters cortical network activity of sensory processing, in which inhibitory input from M1 to S1 may be involved.

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