Sensory responses in motor cortex neurons during precise motor control

1977 ◽  
Vol 5 (5) ◽  
pp. 267-272 ◽  
Author(s):  
Edward V. Evarts ◽  
Christoph Fromm
2018 ◽  
Author(s):  
James C. Dooley ◽  
Mark S. Blumberg

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.


eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
James C Dooley ◽  
Mark S Blumberg

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.


NeuroImage ◽  
2009 ◽  
Vol 47 ◽  
pp. S173
Author(s):  
K Jerbi ◽  
H Hui ◽  
D Pantazis ◽  
J-P Lachaux ◽  
O Bertrand ◽  
...  

Author(s):  
David Burke

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.


2010 ◽  
Vol 104 (5) ◽  
pp. 2873-2885 ◽  
Author(s):  
Suresh D. Muthukumaraswamy

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.


2011 ◽  
Vol 106 (5) ◽  
pp. 2216-2231 ◽  
Author(s):  
Patrick L. Sheets ◽  
Benjamin A. Suter ◽  
Taro Kiritani ◽  
C. Savio Chan ◽  
D. James Surmeier ◽  
...  

Motor cortex is a key brain center involved in motor control in rodents and other mammals, but specific intracortical mechanisms at the microcircuit level are largely unknown. Neuronal expression of hyperpolarization-activated current ( Ih) is cell class specific throughout the nervous system, but in neocortex, where pyramidal neurons are classified in various ways, a systematic pattern of expression has not been identified. We tested whether Ih is differentially expressed among projection classes of pyramidal neurons in mouse motor cortex. Ih expression was high in corticospinal neurons and low in corticostriatal and corticocortical neurons, a pattern mirrored by mRNA levels for HCN1 and Trip8b subunits. Optical mapping experiments showed that Ih attenuated glutamatergic responses evoked across the apical and basal dendritic arbors of corticospinal but not corticostriatal neurons. Due to Ih, corticospinal neurons resonated, with a broad peak at ∼4 Hz, and were selectively modulated by α-adrenergic stimulation. Ih reduced the summation of short trains of artificial excitatory postsynaptic potentials (EPSPs) injected at the soma, and similar effects were observed for short trains of actual EPSPs evoked from layer 2/3 neurons. Ih narrowed the coincidence detection window for EPSPs arriving from separate layer 2/3 inputs, indicating that the dampening effect of Ih extended to spatially disperse inputs. To test the role of corticospinal Ih in transforming EPSPs into action potentials, we transfected layer 2/3 pyramidal neurons with channelrhodopsin-2 and used rapid photostimulation across multiple sites to synaptically drive spiking activity in postsynaptic neurons. Blocking Ih increased layer 2/3-driven spiking in corticospinal but not corticostriatal neurons. Our results imply that Ih-dependent synaptic integration in corticospinal neurons constitutes an intracortical control mechanism, regulating the efficacy with which local activity in motor cortex is transferred to downstream circuits in the spinal cord. We speculate that modulation of Ih in corticospinal neurons could provide a microcircuit-level mechanism involved in translating action planning into action execution.


2019 ◽  
Author(s):  
Tejapratap Bollu ◽  
Brendan Ito ◽  
Sam C. Whitehead ◽  
Brian Kardon ◽  
James Redd ◽  
...  

Abstract:Precise tongue control is necessary for drinking, eating, and vocalizing1, 2. Yet because tongue movements are fast and difficult to resolve, neural control of lingual kinematics remains poorly understood. Here we combine kilohertz frame-rate imaging and a deep learning based neural network to resolve 3D tongue kinematics in mice drinking from a water spout. Successful licks required previously unobserved corrective submovements (CSMs) which, like online corrections during primate reaches3–10, occurred after the tongue missed unseen, distant, or displaced targets. Photoinhibition of anterolateral motor cortex (ALM) impaired online corrections, resulting in hypometric licks that missed the spout. ALM neural activity reflected upcoming, ongoing, and past CSMs, as well as errors in predicted spout contact. Though less than a tenth of a second in duration, a single mouse lick exhibits hallmarks of online motor control associated with a primate reach, including cortex-dependent corrections after misses.


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