scholarly journals Computational neural network provides naturalistic solution for recovery of finger dexterity after stroke

2021 ◽  
Author(s):  
Ashraf Kadry ◽  
Sumner Norman ◽  
Jing Xu ◽  
Deborah Solomonow-Avnon ◽  
Firas Mawase
Keyword(s):  
Neural Network ◽  
Neural Plasticity ◽  
Cortical Neurons ◽  
Primary Motor Cortex ◽  
Cortical Layer ◽  
Inhibitory Neurons ◽  
Cortical Lesion ◽  
Strength Analysis ◽  
Finger Movement ◽  
Finger Dexterity

Finger dexterity is a fundamental movement skill of humans and the ability to individuate fingers imparts high motor flexibility. Disruption of dexterity due to brain injury imposes a detriment to quality of life, and thus understanding the neurological mechanisms responsible for recovery is imperative for neurorehabilitation. Two neuronal pathways have been proposed to play crucial roles in finger individuation: the corticospinal tract, originating from primary motor cortex and premotor areas, and the subcortical reticulospinal tract, originating from the reticular formation in the brainstem. Finger individuation in patients with lesions to these pathways may recover, however it remains an open question how the cortical-reticular network reorganizes and contributes to this recovery following a stroke. We explored the hypothesis that interactive connections between cortical and subcortical neurons reflect dynamics appropriate for generating outgoing commands for finger movement. To formalize this hypothesis, we developed an Artificial Neural Network (ANN) representing the premotor planning input layer, cortical layer including excitatory and inhibitory neurons and reticular layer that control motoneurons eliciting unilateral flexion of two fingers. The ANN was trained to reproduce normal activity of finger individuation and strength. Analysis of the trained ANN revealed that the natural dynamical solution was a near-linear relationship between the force of the instructed and uninstructed finger, resembling individuation patterns in humans. We then applied a simulated stroke lesion to the ANN and explored the resulting finger dexterity at multiple stages post stroke. Analysis revealed: (1) increased unintended force produced by uninstructed fingers (i.e., enslaving) and (2) weakening of the force in the instructed finger immediately after stroke, (3) improved finger control during recovery that typically occurs early after stroke, and (4) association of this behavior with increased neural plasticity of the residual neurons, as reflected by strengthening of connectivity weights between premotor and focal cortical excitatory and inhibitory neurons, but reduction in connectivity in shared cortical neurons. Interestingly, the network solution predicted that the reticulospinal pathway also contributed to the improved behavior. Lastly, the ANN also predicts the effect of cortical lesion size on finger individuation. Our model provides a framework by which to understand a number of experimental findings. The model solution suggests that a key mechanism of finger individuation is establishment of an interactive relationship between cortical and subcortical regions, appropriate to produce desired finger movement.

A Model of Reaching Dynamics in Primary Motor Cortex

1998 ◽  
Vol 10 (1) ◽  
pp. 35-45 ◽  
Author(s):  
Sohie Lee Moody ◽  
David Zipser
Keyword(s):  
Neural Network ◽  
Motor Cortex ◽  
Recurrent Neural Network ◽  
Cortical Neurons ◽  
Primary Motor Cortex ◽  
Voluntary Movements ◽  
Reaching Movement ◽  
Time Constants ◽  
Movement Representation ◽  
The Individual

Features of virtually all voluntary movements are represented in the primary motor cortex. The movements can be ongoing, imminent, delayed, or imagined. Our goal was to investigate the dynamics of movement representation in the motor cortex. To do this we trained a fully recurrent neural network to continually output the direction and magnitude of movements required to reach randomly changing targets. Model neurons developed preferred directions and other properties similar to real motor cortical neurons. The key finding is that when the target for a reaching movement changes location, the ensemble representation of the movement changes nearly monotonically, and the individual neurons comprising the representation exhibit strong, nonmonotonic transients. These transients serve as internal recurrent signals that force the ensemble representation to change more rapidly than if it were limited by the time constants of individual neurons. These transients, if they exist, could be observed in experiments that require only slight modifications of the standard paradigm used to investigate movement representation in the motor cortex.

scholarly journals Cortical and Striatal Electroencephalograms and Apomorphine Effects in the FUS Mouse Model of Amyotrophic Lateral Sclerosis

2021 ◽  
pp. 1-15
Author(s):  
Vasily Vorobyov ◽  
Alexander Deev ◽  
Frank Sengpiel ◽  
Vladimir Nebogatikov ◽  
Aleksey A. Ustyugov
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Motor Neurons ◽  
Cortical Neurons ◽  
Primary Motor Cortex ◽  
Beta Activity ◽  
Systemic Injection ◽  
Eeg Spectra ◽  
Electroencephalogram Eeg ◽  
Lateral Sclerosis

Background: Amyotrophic lateral sclerosis (ALS) is characterized by degeneration of motor neurons resulting in muscle atrophy. In contrast to the lower motor neurons, the role of upper (cortical) neurons in ALS is yet unclear. Maturation of locomotor networks is supported by dopaminergic (DA) projections from substantia nigra to the spinal cord and striatum. Objective: To examine the contribution of DA mediation in the striatum-cortex networks in ALS progression. Methods: We studied electroencephalogram (EEG) from striatal putamen (Pt) and primary motor cortex (M1) in ΔFUS(1–359)-transgenic (Tg) mice, a model of ALS. EEG from M1 and Pt were recorded in freely moving young (2-month-old) and older (5-month-old) Tg and non-transgenic (nTg) mice. EEG spectra were analyzed for 30 min before and for 60 min after systemic injection of a DA mimetic, apomorphine (APO), and saline. Results: In young Tg versus nTg mice, baseline EEG spectra in M1 were comparable, whereas in Pt, beta activity in Tg mice was enhanced. In older Tg versus nTg mice, beta dominated in EEG from both M1 and Pt, whereas theta and delta 2 activities were reduced. In younger Tg versus nTg mice, APO increased theta and decreased beta 2 predominantly in M1. In older mice, APO effects in these frequency bands were inversed and accompanied by enhanced delta 2 and attenuated alpha in Tg versus nTg mice. Conclusion: We suggest that revealed EEG modifications in ΔFUS(1–359)-transgenic mice are associated with early alterations in the striatum-cortex interrelations and DA transmission followed by adaptive intracerebral transformations.

Networks with lateral connectivity. III. Plasticity and reorganization of somatosensory cortex

1996 ◽  
Vol 75 (1) ◽  
pp. 217-232 ◽  
Author(s):  
J. Xing ◽  
G. L. Gerstein
Keyword(s):  
Spontaneous Activity ◽  
Network Model ◽  
Training Stimulus ◽  
Receptive Fields ◽  
Cortical Layer ◽  
Cortical Reorganization ◽  
Cortical Lesion ◽  
Behavioral Training ◽  
Dynamic Changes ◽  
Neuronal Groups

1. Mechanisms underlying cortical reorganizations were studied using a three-layered neural network model with neuronal groups already formed in the cortical layer. 2. Dynamic changes induced in cortex by behavioral training or intracortical microstimulation (ICMS) were simulated. Both manipulations resulted in reassembly of neuronal groups and formation of stimulus-dependent assemblies. Receptive fields of neurons and cortical representation of inputs also changed. Many neurons that had been weakly responsive or silent became active. 3. Several types of learning models were examined in simulating behavioral training, ICMS-induced dynamic changes, deafferentation, or cortical lesion. Each learning model most accurately reproduced features of experimental data from different manipulations, suggesting that more than one plasticity mechanism might be able to induce dynamic changes in cortex. 4. After skin or cortical stimulation ceased, as spontaneous activity continued, the stimulus-dependent assemblies gradually reverted into structure-dependent neuronal groups. However, relationships among individual neurons and identities of many neurons did not return to their original states. Thus a different set of neurons would be recruited by the same training stimulus sequence on its next presentation. 5. We also reproduced several typical long-term reorganizations caused by pathological manipulations such as cortical lesions, input loss, and digit fusion. 6. In summary, with Hebbian plasticity rules on lateral connections, the network model is capable of reproducing most characteristics of experiments on cortical reorganization. We propose that an important mechanism underlying cortical plastic changes is formation of temporary assemblies that are related to receipt of strongly synchronized localized input. Such stimulus-dependent assemblies can be dissolved by spontaneous activity after removal of the stimuli.

scholarly journals Fast-spiking GABA circuit dynamics in the auditory cortex predict recovery of sensory processing following peripheral nerve damage

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Jennifer Resnik ◽  
Daniel B Polley
Keyword(s):  
Peripheral Nerve ◽  
Auditory Cortex ◽  
Sensory Processing ◽  
Cortical Neurons ◽  
Sensory Nerve ◽  
Intracortical Inhibition ◽  
Nerve Fibers ◽  
Nerve Damage ◽  
Inhibitory Neurons ◽  
Sound Processing

Cortical neurons remap their receptive fields and rescale sensitivity to spared peripheral inputs following sensory nerve damage. To address how these plasticity processes are coordinated over the course of functional recovery, we tracked receptive field reorganization, spontaneous activity, and response gain from individual principal neurons in the adult mouse auditory cortex over a 50-day period surrounding either moderate or massive auditory nerve damage. We related the day-by-day recovery of sound processing to dynamic changes in the strength of intracortical inhibition from parvalbumin-expressing (PV) inhibitory neurons. Whereas the status of brainstem-evoked potentials did not predict the recovery of sensory responses to surviving nerve fibers, homeostatic adjustments in PV-mediated inhibition during the first days following injury could predict the eventual recovery of cortical sound processing weeks later. These findings underscore the potential importance of self-regulated inhibitory dynamics for the restoration of sensory processing in excitatory neurons following peripheral nerve injuries.

scholarly journals Astrocytic modulation of information processing by layer 5 pyramidal neurons of the mouse visual cortex

2020 ◽  
Author(s):  
Dimitri Ryczko ◽  
Maroua Hanini-Daoud ◽  
Steven Condamine ◽  
Benjamin J. B. Bréant ◽  
Maxime Fougère ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Cortical Neurons ◽  
Calcium Binding ◽  
Pyramidal Neurons ◽  
Binding Protein ◽  
Contextual Information ◽  
Dendritic Tree ◽  
Cortical Layer ◽  
List Type ◽  
Ionic Environment

AbstractThe most complex cerebral functions are performed by the cortex which most important output is carried out by its layer 5 pyramidal neurons. Their firing reflects integration of sensory and contextual information that they receive. There is evidence that astrocytes influence cortical neurons firing through the release of gliotransmitters such as ATP, glutamate or GABA. These effects were described at the network and at the synaptic levels, but it is still unclear how astrocytes influence neurons input-output transfer function at the cellular level. Here, we used optogenetic tools coupled with electrophysiological, imaging and anatomical approaches to test whether and how astrocytic activation affected processing and integration of distal inputs to layer 5 pyramidal neurons (L5PN). We show that optogenetic activation of astrocytes near L5PN cell body prolonged firing induced by distal inputs to L5PN and potentiated their ability to trigger spikes. The observed astrocytic effects on L5PN firing involved glutamatergic transmission to some extent but relied on release of S100β, an astrocytic Ca2+-binding protein that decreases extracellular Ca2+ once released. This astrocyte-evoked decrease of extracellular Ca2+ elicited firing mediated by activation of Nav1.6 channels. Our findings suggest that astrocytes contribute to the cortical fundamental computational operations by controlling the extracellular ionic environment.Key Points SummaryIntegration of inputs along the dendritic tree of layer 5 pyramidal neurons is an essential operation as these cells represent the most important output carrier of the cerebral cortex. However, the contribution of astrocytes, a type of glial cell to these operations is poorly documented.Here we found that optogenetic activation of astrocytes in the vicinity of layer 5 in the mouse primary visual cortex induce spiking in local pyramidal neurons through Nav1.6 ion channels and prolongs the responses elicited in these neurons by stimulation of their distal inputs in cortical layer 1.This effect partially involved glutamatergic signalling but relied mostly on the astrocytic calcium-binding protein S100β, which regulates the concentration of calcium in the extracellular space around neurons.These findings show that astrocytes contribute to the fundamental computational operations of the cortex by acting on the ionic environment of neurons.

scholarly journals Subanesthetic ketamine reactivates adult cortical plasticity to restore vision from amblyopia

2020 ◽  
Author(s):  
Steven F. Grieco ◽  
Xin Qiao ◽  
Xiaoting Zheng ◽  
Yongjun Liu ◽  
Lujia Chen ◽  
...  
Keyword(s):  
Functional Recovery ◽  
Neural Plasticity ◽  
Cortical Plasticity ◽  
Brain Plasticity ◽  
Excitatory Input ◽  
Inhibitory Neurons ◽  
List Type ◽  
Visual Cortical

SummarySubanesthetic ketamine evokes rapid and long-lasting antidepressant effects in human patients. The mechanism for ketamine’s effects remains elusive, but ketamine may broadly modulate brain plasticity processes. We show that single-dose ketamine reactivates adult mouse visual cortical plasticity and promotes functional recovery of visual acuity defects from amblyopia. Ketamine specifically induces down-regulation of neuregulin-1 (NRG1) expression in parvalbumin-expressing (PV) inhibitory neurons in mouse visual cortex. NRG1 downregulation in PV neurons co-tracks both the fast onset and sustained decreases in synaptic inhibition to excitatory neurons, along with reduced synaptic excitation to PV neurons in vitro and in vivo following a single ketamine treatment. These effects are blocked by exogenous NRG1 as well as PV targeted receptor knockout. Thus ketamine reactivation of adult visual cortical plasticity is mediated through rapid and sustained cortical disinhibition via downregulation of PV-specific NRG1 signaling. Our findings reveal the neural plasticity-based mechanism for ketamine-mediated functional recovery from adult amblyopia.Highlights○ Disinhibition of excitatory cells by ketamine occurs in a fast and sustained manner○ Ketamine evokes NRG1 downregulation and excitatory input loss to PV cells○ Ketamine induced plasticity is blocked by exogenous NRG1 or its receptor knockout○ PV inhibitory cells are the initial functional locus underlying ketamine’s effects

Two movement-related foci in the primate cingulate cortex observed in signal-triggered and self-paced forelimb movements

1991 ◽  
Vol 65 (2) ◽  
pp. 188-202 ◽  
Author(s):  
K. Shima ◽  
K. Aya ◽  
H. Mushiake ◽  
M. Inase ◽  
H. Aizawa ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Primary Motor Cortex ◽  
Motor Task ◽  
Cingulate Cortex ◽  
Posterior Cingulate Cortex ◽  
The Self ◽  
Anterior Cingulate ◽  
Key Press ◽  
Flexor Muscles ◽  
Hrp Method

1. Single-unit activity in the cingulate cortex of the monkey was recorded during the performance of sensorially (visual, auditory, or tactile) triggered or self-paced forelimb key press movements. 2. Microelectrodes were inserted into the broad rostrocaudal expanse of the cingulate cortex, including the upper and lower banks of the cingulate sulcus and the hemispheric medial wall of the cingulate gyrus. 3. A total of 1,042 task-related neurons were examined, the majority of which were related to the execution of the key press movements. In greater than 60% of them, the movement-related activity preceded the activity in the distal flexor muscles. 4. The movement-related neurons were distributed, in two foci, in the posterior and anterior parts of the cingulate cortex, both including the upper and lower banks of the cingulate sulcus. The posterior focus was found to largely overlap the area projecting to the forelimb area of the primary motor cortex by the use of the horseradish peroxidase (HRP) method. 5. About 40% of the cingulate cortical neurons showed equimagnitude responses during the signal-triggered and self-paced movements. The neurons exhibiting a selective or differential response to the self-paced motor task were more frequently observed in the anterior than in the posterior cingulate cortex. 6. The long-lead type of changes in activity, ranging from 500 ms to 2 s, were observed mainly before the self-paced and, much less frequently, before the triggered movements. They were particularly abundant in the anterior cingulate cortex. 7. Only a few of the neurons showed activity time-locked to the onset of the sensory signals. 8. These observations indicate that the anterior and posterior parts of the cingulate cortex are distinct entities participating in the performance of limb movements, even if the movements are simple, such as those in this study.

Segmentation, Binding, and Illusory Conjunctions

1991 ◽  
Vol 3 (4) ◽  
pp. 510-525 ◽  
Author(s):  
D. Horn ◽  
D. Sagi ◽  
M. Usher
Keyword(s):  
Neural Network ◽  
Human Vision ◽  
Inhibitory Neurons ◽  
Cell Assemblies ◽  
Inhibitory Cell ◽  
Excitatory Cell ◽  
Illusory Conjunctions

We investigate binding within the framework of a model of excitatory and inhibitory cell assemblies that form an oscillating neural network. Our model is composed of two such networks that are connected through their inhibitory neurons. The excitatory cell assemblies represent memory patterns. The latter have different meanings in the two networks, representing two different attributes of an object, such as shape and color. The networks segment an input that contains mixtures of such pairs into staggered oscillations of the relevant activities. Moreover, the phases of the oscillating activities representing the two attributes in each pair lock with each other to demonstrate binding. The system works very well for two inputs, but displays faulty correlations when the number of objects is larger than two. In other words, the network conjoins attributes of different objects, thus showing the phenomenon of “illusory conjunctions,” as in human vision.

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