Neuronal activity reorganization in motor cortex for successful locomotion after a lesion in the ventrolateral thalamus

Author(s):  
Irina N. Beloozerova

Thalamic stroke leads to ataxia if the cerebellum-receiving ventrolateral thalamus (VL) is affected. The compensation mechanisms for this deficit are not well understood, particularly the roles that single neurons and specific neuronal subpopulations outside the thalamus play in recovery. The goal of this study was to clarify neuronal mechanisms of the motor cortex involved in mitigation of ataxia during locomotion when part of the VL is inactivated or lesioned. In freely ambulating cats, we recorded the activity of neurons in layer V of the motor cortex as the cats walked on a flat surface and horizontally placed ladder. We first reversibly inactivated approximately 10% of the VL unilaterally using glutamatergic transmission antagonist CNQX and analyzed how the activity of motor cortex reorganized to support successful locomotion. We next lesioned 50-75% of the VL bilaterally using kainic acid and analyzed how the activity of motor cortex reorganized when locomotion recovered. When a small part of the VL was inactivated, the discharge rates of motor cortex neurons decreased, but otherwise the activity was near normal, and the cats walked fairly well. Individual neurons retained their ability to respond to the demand for accuracy during ladder locomotion; however, most changed their response. When the VL was lesioned, the cat walked normally on the flat surface but was ataxic on the ladder for several days post-lesion. When ladder locomotion normalized, neuronal discharge rates on the ladder were normal, and the shoulder-related group was preferentially active during the stride's swing phase.

2011 ◽  
Vol 106 (5) ◽  
pp. 2688-2697 ◽  
Author(s):  
Francesco Negro ◽  
Dario Farina

Oscillations in the primary motor cortex are transmitted through the corticospinal tract to the motoneuron pool. This pathway is believed to produce an effective and direct command from the motor cortex to the spinal motoneurons for the modulation of the force output. In this study, we used a computational model of a population of motoneurons to investigate the factors that can influence the transmission of the cortical input to the output of motoneurons, since it can be quantified by coherence analysis. The simulations demonstrated that, despite the nonlinearity of the motoneurons, oscillations present in the cortical input are transmitted to the output of the motoneuron pool at the same frequency. However, the interference introduced by the nonlinearity of the system increases the variability of the oscillations in output, introducing spectral lines whose frequency depends on the input frequencies and the motoneuron discharge rates. Moreover, an additional source of synaptic input common to all motoneurons but independent from the corticospinal component decorrelates the cortical input and motoneuron output and, thus, decreases the magnitude of the estimated coherence, even if the effective cortical drive does not change. These results indicate that the corticospinal input can effectively be sampled by a small population of motoneurons. However, the transmission of a corticospinal drive to the motoneuron pool is influenced by the nonlinearity of the spiking processes of the active motoneurons and by synaptic inputs common to the motoneuron population but independent from the cortical input.


Resuscitation ◽  
1997 ◽  
Vol 35 (2) ◽  
pp. 157-164 ◽  
Author(s):  
Victor A Akulinin ◽  
Sergey S Stepanov ◽  
Valeriy V Semchenko ◽  
Pavel V Belichenko

Author(s):  
Juan A. Barios ◽  
Santiago Ezquerro ◽  
Arturo Bertomeu-Motos ◽  
Jose M. Catalan ◽  
Jose M. Sanchez-Aparicio ◽  
...  

Conventional rehabilitation strategies for stroke survivors become difficult when voluntary movements are severely disturbed. Combining passive limb mobilization, robotic devices and EEG-based brain-computer interfaces (BCI) systems might improve treatment and clinical follow-up of these patients, but detailed knowledge of neurophysiological mechanisms involved in functional recovery, which might help for tailoring stroke treatment strategies, is lacking. Movement-related EEG changes (EEG event-related desynchronization (ERD) in [Formula: see text] and [Formula: see text] bands, an indicator of motor cortex activation traditionally used for BCI systems), were evaluated in a group of 23 paralyzed chronic stroke patients in two unilateral motor tasks alternating paretic and healthy hands ((i) passive movement, using a hand exoskeleton, and (ii) voluntary movement), and compared to nine healthy subjects. In tasks using unaffected hand, we observed an increase of contralesional hemisphere activation for stroke patients group. Unexpectedly, when using paralyzed hand, motor cortex activation was reduced or absent in severely affected group of patients, while patients with moderate motor deficit showed an activation greater than control group. Cortical activation was reduced or absent in damaged hemisphere of all the patients in both tasks. Significant differences related to severity of motor deficit were found in the time course of [Formula: see text] bands power ratio in EEG of contralesional hemisphere while moving affected hand. These findings suggest the presence of different compensation mechanisms in contralesional hemisphere of stroke patients related to the grade of motor disability, that might turn quantitative EEG during a movement task, obtained from a BCI system controlling a robotic device included in a rehabilitation task, into a valuable tool for monitoring clinical progression, evaluating recovery, and tailoring treatment of stroke patients.


1976 ◽  
Vol 39 (5) ◽  
pp. 1020-1031 ◽  
Author(s):  
P. L. Strick

1. The origin and topographical organization of input to the arm area of the primate motor cortex from the ventrolateral thalamus were examined using the method of retrograde transport of horseradish peroxidase (HRP). 2. A thin, continuous slab of labeled neurons was found in the ventrolateral thalamus followingmultiple injections of HRP into the arm area of the motor cortex. The slab of labeled neurons was flanked, medially and laterally, by groups of unlabeled neurons. 3. The origin of ventrolateral thalamic input was more extensive than previously thought. Labeled neurons were found from A10.0 to A6.0 and occurred in three ventolateral thalamic subdivisions: ventralis lateralis pars oralis (VLo), ventralis lateralis pars caudalis (VLc), and ventralis posterior lateralis pars oralis (VPLo). For simplicity this region containing labeled neurons has been termed the ventrolateral thalamic (VL) arm area. 4. Injections of HRP into the somatic sensory cortex indicated that the thalamic regions which project to the somatic sensory cortex are separate from the VL arm area. 5. The distribution of labeled neurons following single injections of HRP into different regions of the motor cortex arm area indicated that the VL arm area is topographically organized, particularly its caudal part. Ventral regions of the VL arm area were labeled following HRP injections into motor cortex regions adjacent to the central sulcus where the representation of largely distal musculature is localized. Dorsal regions of the VL arm area were labeled following HRP injections into motor cortex regions more rostral to the central sulcus where the representation of more proximal musculature is localized. 6. A larger region of the VL arm area was labeled following HRP injections adjacent to the central sulcus than following the more rostral motor cortex injections. This suggests that, like the arm area of the motor cortex, more of the VL arm area is allotted to the representation of distal than proximal musculature. 7. Following very small cortical HRP injections, isolated labeled thalamic neurons were diffusely scattered throughout a 3-mm rostrocaudal extent of the VL arm area. In addition, a small focal cluster of labeled thalamic neurons was also seen. The labeled cluster was limited to 0.5 mm rostrocaudally and 300 mum in width. The focal distribution of labeled thalamic neurons suggests that aspects of a point to point organization may exist in the connection between VL and the motor cortex arm area.


2009 ◽  
Vol 102 (2) ◽  
pp. 1026-1039 ◽  
Author(s):  
W. S. Smith ◽  
E. E. Fetz

We investigated the synaptic interactions between neighboring motor cortex cells in monkeys generating isometric ramp-and-hold torques about the wrist. For pairs of cortical cells the response patterns were determined in response-aligned averages and their synaptic interactions were identified by cross-correlation histograms. Cross-correlograms were compiled for 215 cell pairs and 84 (39%) showed significant features. The most frequently found feature (65/84 = 77%) was a central peak, straddling the origin and representing a source of common synaptic input to both cells. One third of these also had superimposed lagged peaks, indicative of a serial excitatory connection. Pure lagged peaks and lagged troughs, indicative of serial excitatory or inhibitory linkages, respectively, both occurred in 5% of the correlograms with features. A central trough appeared in 13% of the correlograms. The magnitude of the synaptic linkage was measured as the normalized area of the correlogram feature. Plotting the strength of synaptic interaction against response similarity during alternating wrist torques revealed a positive relationship for the correlated cell pairs. A linear fit yielded a positive slope: the pairs with excitatory interactions tended to covary more often than countervary. This linear fit had a positive offset, reflecting a tendency for both covarying and countervarying cells to have excitatory common input. Plotting the cortical location of the cell pairs showed that the strongest interactions occurred between cells separated by <400 microns. The correlational linkages between cells of different cortical layers showed a large proportion of common input to cells in layer V.


2020 ◽  
Vol 40 (33) ◽  
pp. 6289-6308 ◽  
Author(s):  
Thomas Andreska ◽  
Stefanie Rauskolb ◽  
Nina Schukraft ◽  
Patrick Lüningschrör ◽  
Manju Sasi ◽  
...  

2019 ◽  
Author(s):  
Jérémy Cousineau ◽  
Léa Lescouzères ◽  
Anne Taupignon ◽  
Lorena Delgado-Zabalza ◽  
Emmanuel Valjent ◽  
...  

AbstractDopamine (DA) plays a crucial role in the control of motor and higher cognitive functions such as learning, working memory and decision making. The primary motor cortex (M1), which is essential for motor control and the acquisition of motor skills, receives dopaminergic inputs in its superficial and deep layers from the midbrain. However, the precise action of DA and DA receptor subtypes on the cortical microcircuits of M1 remains poorly understood. The aim of this work was to investigate how DA, through the activation of D2 receptors (D2R), modulates the cellular and synaptic activity of M1 parvalbumin-expressing interneurons (PVINs) which are crucial to regulate the spike output of pyramidal neurons (PNs). By combining immunofluorescence, ex vivo electrophysiology, pharmacology and optogenetics approaches, we show that D2R activation increases neuronal excitability of PVINs and GABAergic synaptic transmission between PVINs and PNs in layer V of M1. Our data reveal a mechanism through which cortical DA modulates M1 microcircuitry and might participate in the acquisition of motor skills.Significance StatementPrimary motor cortex (M1), which is a region essential for motor control and the acquisition of motor skills, receives dopaminergic inputs from the midbrain. However, precise action of dopamine and its receptor subtypes on specific cell types in M1 remained poorly understood. Here, we demonstrate in M1 that dopamine D2 receptors (D2R) are present in parvalbumin interneurons (PVINs) and their activation increases the excitability of the PVINs, which are crucial to regulate the spike output of pyramidal neurons (PNs). Moreover the activation of the D2R facilitates the GABAergic synaptic transmission of those PVINs on layer V PNs. These results highlight how cortical dopamine modulates the functioning of M1 microcircuit which activity is disturbed in hypo- and hyperdopaminergic states.


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