scholarly journals Disengagement of motor cortex from movement control during long-term learning

2019 ◽  
Vol 5 (10) ◽  
pp. eaay0001 ◽  
Author(s):  
Eun Jung Hwang ◽  
Jeffrey E. Dahlen ◽  
Yvonne Yuling Hu ◽  
Karina Aguilar ◽  
Bin Yu ◽  
...  

Motor learning involves reorganization of the primary motor cortex (M1). However, it remains unclear how the involvement of M1 in movement control changes during long-term learning. To address this, we trained mice in a forelimb-based motor task over months and performed optogenetic inactivation and two-photon calcium imaging in M1 during the long-term training. We found that M1 inactivation impaired the forelimb movements in the early and middle stages, but not in the late stage, indicating that the movements that initially required M1 became independent of M1. As previously shown, M1 population activity became more consistent across trials from the early to middle stage while task performance rapidly improved. However, from the middle to late stage, M1 population activity became again variable despite consistent expert behaviors. This later decline in activity consistency suggests dissociation between M1 and movements. These findings suggest that long-term motor learning can disengage M1 from movement control.

2014 ◽  
Vol 111 (5) ◽  
pp. 897-899 ◽  
Author(s):  
Mark R. Hinder ◽  
Paola Reissig ◽  
Hakuei Fujiyama

Seminal work in animals indicates that learning a motor task results in long-term potentiation (LTP) in primary motor cortex (M1) and a subsequent occlusion of LTP induction (Rioult-Pedotti et al. J Neurophysiol 98: 3688–3695, 2007). Using various forms of noninvasive brain stimulation in conjunction with a motor learning paradigm, Cantarero et al. ( J Neurosci 33: 12862–12869, 2013) recently provided novel evidence to support the hypothesis that retention of motor skill is contingent upon this postlearning occlusion.


2005 ◽  
Vol 93 (3) ◽  
pp. 1486-1497 ◽  
Author(s):  
Jeremy D. Cohen ◽  
Manuel A. Castro-Alamancos

Learning of motor skills may occur as a consequence of changes in the efficacy of synaptic connections in the primary motor cortex. We investigated if learning in a reaching task affects the excitability, short-term plasticity, and long-term plasticity of horizontal connections in layers II–III of the motor cortex. Because training in this task requires animals to be food-deprived, we compared the trained animals with similarly food-deprived untrained animals and normal controls. The results show that the excitability, short-term plasticity, and long-term plasticity of the studied horizontal connections were unaffected by motor learning. However, stress-related effects produced by food deprivation and handling significantly enhanced the expression of long-term depression in these pathways. These results are compatible with the hypothesis that the acquisition of a complex motor skill produces bi-directional changes in synaptic strength that are distributed throughout the complex neural networks of motor cortex, which remains synaptically balanced during learning. The results are incompatible with the idea that learning causes large unidirectional changes in the population response of these neural networks, which may occur instead during certain behavioral states, such as stress.


2014 ◽  
Vol 112 (11) ◽  
pp. 2985-3000 ◽  
Author(s):  
Mohsen Omrani ◽  
J. Andrew Pruszynski ◽  
Chantelle D. Murnaghan ◽  
Stephen H. Scott

Corrective responses to external perturbations are sensitive to the behavioral task being performed. It is believed that primary motor cortex (M1) forms part of a transcortical pathway that contributes to this sensitivity. Previous work has identified two distinct phases in the perturbation response of M1 neurons, an initial response starting ∼20 ms after perturbation onset that does not depend on the intended motor action and a task-dependent response that begins ∼40 ms after perturbation onset. However, this invariant initial response may reflect ongoing postural control or a task-independent response to the perturbation. The present study tested these two possibilities by examining if being engaged in an ongoing postural task before perturbation onset modulated the initial perturbation response in M1. Specifically, mechanical perturbations were applied to the shoulder and/or elbow while the monkey maintained its hand at a central target or when it was watching a movie and not required to respond to the perturbation. As expected, corrective movements, muscle stretch responses, and M1 population activity in the late perturbation epoch were all significantly diminished in the movie task. Strikingly, initial perturbation responses (<40 ms postperturbation) remained the same across tasks, suggesting that the initial phase of M1 activity constitutes a task-independent response that is sensitive to the properties of the mechanical perturbation but not the goal of the ongoing motor task.


2019 ◽  
Author(s):  
Jerjian S.J. ◽  
Sahani M. ◽  
Kraskov A.

AbstractPyramidal tract neurons (PTNs) within macaque rostral ventral premotor cortex (F5) and primary motor cortex (M1) provide direct input to spinal circuitry and are critical for skilled movement control, but surprisingly, can also be active during passive action observation. We recorded from single neurons, including identified PTNs in the hand and arm area of primary motor cortex (M1) (n=189), and in premotor area F5 (n=115) of two adult male macaques, while they executed, observed, or simply withheld (NoGo) reach-to-grasp and hold actions. We found that F5 maintains a more sustained, similar representation of grasping actions during both execution and observation. In contrast, although some M1 neurons mirrored during the grasp and hold, M1 population activity during observation contained signatures of a withholding state. This suggests that M1 and its output may dissociates signals required for the initiation of movement from those associated with the representation of grasp in order to flexibly guide behaviour.Significance StatementVentral premotor cortex (area F5) maintains a similar representation of grasping actions during both execution and observation. Primary motor cortex and its outputs dissociate between movement and non-movement states.


2013 ◽  
Vol 110 (5) ◽  
pp. 1180-1189 ◽  
Author(s):  
Gustaf M. Van Acker ◽  
Sommer L. Amundsen ◽  
William G. Messamore ◽  
Hongyu Y. Zhang ◽  
Carl W. Luchies ◽  
...  

High-frequency, long-duration intracortical microstimulation (HFLD-ICMS) applied to motor cortex is recognized as a useful and informative method for corticomotor mapping by evoking natural-appearing movements of the limb to consistent stable end-point positions. An important feature of these movements is that stimulation of a specific site in motor cortex evokes movement to the same spatial end point regardless of the starting position of the limb. The goal of this study was to delineate effective stimulus parameters for evoking forelimb movements to stable spatial end points from HFLD-ICMS applied to primary motor cortex (M1) in awake monkeys. We investigated stimulation of M1 as combinations of frequency (30–400 Hz), amplitude (30–200 μA), and duration (0.5–2 s) while concurrently recording electromyographic (EMG) activity from 24 forelimb muscles and movement kinematics with a motion capture system. Our results suggest a range of parameters (80–140 Hz, 80–140 μA, and 1,000-ms train duration) that are effective and safe for evoking forelimb translocation with subsequent stabilization at a spatial end point. The mean time for stimulation to elicit successful movement of the forelimb to a stable spatial end point was 475.8 ± 170.9 ms. Median successful frequency and amplitude were 110 Hz and 110 μA, respectively. Attenuated parameters resulted in inconsistent, truncated, or undetectable movements, while intensified parameters yielded no change to movement end points and increased potential for large-scale physiological spread and adverse focal motor effects. Establishing cortical stimulation parameters yielding consistent forelimb movements to stable spatial end points forms the basis for a systematic and comprehensive mapping of M1 in terms of evoked movements and associated muscle synergies. Additionally, the results increase our understanding of how the central nervous system may encode movement.


BMJ Open ◽  
2017 ◽  
Vol 7 (8) ◽  
pp. e016566
Author(s):  
Eline C C van Lieshout ◽  
Johanna M A Visser-Meily ◽  
Sebastiaan F W Neggers ◽  
H Bart van der Worp ◽  
Rick M Dijkhuizen

IntroductionMany patients with stroke have moderate to severe long-term sensorimotor impairments, often including inability to execute movements of the affected arm or hand. Limited recovery from stroke may be partly caused by imbalanced interaction between the cerebral hemispheres, with reduced excitability of the ipsilesional motor cortex while excitability of the contralesional motor cortex is increased. Non-invasive brain stimulation with inhibitory repetitive transcranial magnetic stimulation (rTMS) of the contralesional hemisphere may aid in relieving a post-stroke interhemispheric excitability imbalance, which could improve functional recovery. There are encouraging effects of theta burst stimulation (TBS), a form of TMS, in patients with chronic stroke, but evidence on efficacy and long-term effects on arm function of contralesional TBS in patients with subacute hemiparetic stroke is lacking.Methods and analysisIn a randomised clinical trial, we will assign 60 patients with a first-ever ischaemic stroke in the previous 7–14 days and a persistent paresis of one arm to 10 sessions of real stimulation with TBS of the contralesional primary motor cortex or to sham stimulation over a period of 2 weeks. Both types of stimulation will be followed by upper limb training. A subset of patients will undergo five MRI sessions to assess post-stroke brain reorganisation. The primary outcome measure will be the upper limb function score, assessed from grasp, grip, pinch and gross movements in the action research arm test, measured at 3 months after stroke. Patients will be blinded to treatment allocation. The primary outcome at 3 months will also be assessed in a blinded fashion.Ethics and disseminationThe study has been approved by the Medical Research Ethics Committee of the University Medical Center Utrecht, The Netherlands. The results will be disseminated through (open access) peer-reviewed publications, networks of scientists, professionals and the public, and presented at conferences.Trial registration numberNTR6133


2019 ◽  
Vol 696 ◽  
pp. 33-37 ◽  
Author(s):  
Ippei Nojima ◽  
Tatsunori Watanabe ◽  
Tomoya Gyoda ◽  
Hisato Sugata ◽  
Takashi Ikeda ◽  
...  

2018 ◽  
Author(s):  
Johanna Neuner ◽  
Elena Katharina Schulz-Trieglaff ◽  
Sara Gutiérrez-Ángel ◽  
Fabian Hosp ◽  
Matthias Mann ◽  
...  

AbstractHuntington’s disease (HD) is a devastating hereditary movement disorder, characterized by degeneration of neurons in the striatum and cortex. Studies in human patients and mouse HD models suggest that disturbances of neuronal function in the neocortex play an important role in the disease onset and progression. However, the precise nature and time course of cortical alterations in HD have remained elusive. Here, we use chronicin vivotwo-photon calcium imaging to monitor the activity of single neurons in layer 2/3 of the primary motor cortex in awake, behaving R6/2 transgenic HD mice and wildtype littermates. R6/2 mice show age-dependent changes in neuronal activity with a clear increase in activity at the age of 8.5 weeks, preceding the onset of motor and neurological symptoms. Furthermore, quantitative proteomics demonstrate a pronounced downregulation of synaptic proteins in the cortex, and histological analyses in R6/2 mice and HD patient samples reveal reduced inputs from parvalbumin-positive interneurons onto layer 2/3 pyramidal cells. Thus, our study provides a time-resolved description as well as mechanistic details of cortical circuit dysfunction in HD.Significance statementFuntional alterations in the cortex are believed to play an important role in the pathogenesis of Huntington’s disease (HD). However, studies monitoring cortical activity in HD modelsin vivoat a single-cell resultion are still lacking. We have used chronic two-photon imaging to investigate changes in the activity of single neurons in the primary motor cortex of awake presymptomatic HD mice. We show that neuronal activity increases before the mice develop disease symptoms. Our histological analyses in mice and in human HD autopsy cases furthermore demonstrate a loss inhibitory synaptic terminals from parvalbimun-positive interneurons, revealing a potential mechanism of cortical circuit impairment in HD.


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