More conditioning stimuli enhance synaptic plasticity in the human spinal cord

Fitzpatrick, Siobhan C.; Luu, Billy L.; Butler, Jane E.; Taylor, Janet L.

doi:10.1016/j.clinph.2015.03.013

Cited by 27 publications

(26 citation statements)

References 35 publications

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“…This caused us to analyse our results simply by combining responses to all stimuli given after the intervention. It is possible that longer periods of stimulation with MI could enhance plastic changes and lead to a more consistent and long-lasting increase in MEPs, as has been reported with other paradigms (Fitzpatrick et al 2016). This would allow a more detailed examination of the time scale of the changes in future.…”

Section: Motor Imagery With Tms Induced Plasticitymentioning

confidence: 73%

Induction of plasticity in the human motor system by motor imagery and transcranial magnetic stimulation

Foysal

Baker

2020

The Journal of Physiology

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Key points Delivering transcranial magnetic brain stimulation over the motor cortex during motor imagination leads to enhanced motor output, which is selective for the muscles primarily involved in the imagined movement. This novel protocol may be useful to enhance function after damage to the motor system, such as after stroke. Abstract Several paired stimulation paradigms are known to induce plasticity in the motor cortex, reflected by changes in the motor evoked potential (MEP) following the paired stimulation. Motor imagery (MI) is capable of activating the motor system and affecting cortical excitability. We hypothesized that it might be possible to use MI in conjunction with transcranial magnetic stimulation (TMS) to induce plasticity in the human motor system. TMS was delivered to the motor cortex of healthy human subjects, and baseline MEPs recorded from forearm flexor, forearm extensor and intrinsic hand muscles. Subjects were then asked to imagine either wrist flexion or extension movements during TMS delivery (n = 90 trials). Immediately after this intervention, MEP measurement was repeated. Control protocols tested the impact of imagination or TMS alone. Flexion imagination with TMS increased MEPs in flexors and an intrinsic hand muscle. Extensor imagination with TMS increased MEPs in extensor muscles only. The control paradigms did not produce significant changes. We conclude that delivering TMS during MI is capable of inducing plastic changes in the motor system. This new protocol may find utility to enhance functional rehabilitation after brain injury.

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Section: Motor Imagery With Tms Induced Plasticitymentioning

confidence: 73%

Induction of plasticity in the human motor system by motor imagery and transcranial magnetic stimulation

Foysal

Baker

2020

The Journal of Physiology

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“…This leaves three possible sites of action: Either excitability changes are generated in the soma or axons of the corticospinal neurons of the primary motor cortex or changes in transmission occur across their terminals in the spinal cord. The latter possibility should not be fully excluded, since evidence of changes in the efficiency of corticospinal terminals in the spinal cord has been demonstrated in relation to changes in arm posture (Donges, Taylor, & Nuzzo, 2019;Nuzzo, Trajano, Barry, Gandevia, & Taylor, 2016) and plasticity-inducing stimulation protocols (Fitzpatrick, Luu, Butler, & Taylor, 2016;Taube, Leukel, Nielsen, & Lundbye-Jensen, 2015). However, it would require that the current from tsDCS reaches the ventral part of the spinal cord, which is doubtful and it fails to explain why only terminals from descending fibers were influenced, whereas Ia afferent terminals were unaffected judged by the lack of effect of tsDCS on the H-reflex.…”

Section: Evidence Of Increased Corticospinal Drive To Spinal Motor mentioning

confidence: 99%

Transcutaneous spinal direct current stimulation increases corticospinal transmission and enhances voluntary motor output in humans

et al. 2020

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Optimization of motor performance is of importance in daily life, in relation to recovery following injury as well as for elite sports performance. The present study investigated whether transcutaneous spinal direct current stimulation (tsDCS) may enhance voluntary ballistic activation of ankle muscles and descending activation of spinal motor neurons in able‐bodied adults. Forty‐one adults (21 men; 24.0 ± 3.2 years) participated in the study. The effect of tsDCS on ballistic motor performance and plantar flexor muscle activation was assessed in a double‐blinded sham‐controlled cross‐over experiment. In separate experiments, the underlying changes in excitability of corticospinal and spinal pathways were probed by evaluating soleus (SOL) motor evoked potentials (MEPs) following single‐pulse transcranial magnetic stimulation (TMS) over the primary motor cortex, SOL H‐reflexes elicited by tibial nerve stimulation and TMS‐conditioning of SOL H‐reflexes. Measures were obtained before and after cathodal tsDCS over the thoracic spine (T11‐T12) for 10 min at 2.5 mA. We found that cathodal tsDCS transiently facilitated peak acceleration in the ballistic motor task compared to sham tsDCS. Following tsDCS, SOL MEPs were increased without changes in H‐reflex amplitudes. The short‐latency facilitation of the H‐reflex by subthreshold TMS, which is assumed to be mediated by the fast conducting monosynaptic corticomotoneuronal pathway, was also enhanced by tsDCS. We argue that tsDCS briefly facilitates voluntary motor output by increasing descending drive from corticospinal neurones to spinal plantar flexor motor neurons. tsDCS can thus transiently promote within‐session CNS function and voluntary motor output and holds potential as a technique in the rehabilitation of motor function following central nervous lesions.

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“…A likely reason is that neurons in vivo 55 have a much higher background synaptic conductance, which effectively shunt out 56 prominent activation of inherent conductances that may still be inherent in the 57 membrane of the neuron at adult age. This phenomenon has been demonstrated for the 58 deep cerebellar nuclear neurons [29], which have prominent intrinsic conductances in 59 juvenile brain slices, but there intrinsic conductances are normally not activated in vivo. 60 Hence from existing observations in adult mammals in vivo, it would seem that the 61 spinal cord circuitry would have to rely on other self inhibitory mechanisms than spike 62 frequency adaptation or intrinsically generated bursting, and our study assumes this 63 scenario to apply.…”

Section: Introductionmentioning

confidence: 77%

“…In such case, a 286 variety of non specific excitatory input to the spinal cord would be expected to create 287 the types of neural activation patterns that we automatically identify as being 288 compatible with CPGs. Long term synaptic plasticity in the spinal cord has been 289 demonstrated [56][57][58]. The spinal cord is also able to adapt to produce locomotion 290 despite significant experimental changes in muscle insertion sites [59].…”

mentioning

confidence: 99%

Biological data questions the support of the self inhibition required for pattern generation in the half center model

Köhler¹,

Stratmann²,

Röhrbein³

et al. 2019

Preprint

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Locomotion control in mammals has been hypothesized to be governed by a central pattern generator (CPG) located in the circuitry of the spinal cord. The most common model of the CPG is the half center model, where two pools of neurons generate alternating, oscillatory activity. In this model, the pools reciprocally inhibit each other ensuring alternating activity. There is experimental support for reciprocal inhibition. However another crucial part of the half center model is a self inhibitory mechanism which prevents the neurons of each individual pool from infinite firing. Self-inhibition is hence necessary to obtain alternating activity. But critical parts of the experimental bases for the proposed mechanisms for self-inhibition were obtained in vitro, in preparations of juvenile animals. The commonly used adaptation of spike firing does not appear to be present in adult animals in vivo. We therefore modeled several possible self inhibitory mechanisms for locomotor control. Based on currently published data, previously proposed hypotheses of the self inhibitory mechanism, necessary to support the CPG hypothesis, seems to be put into question by functional evaluation tests or by in vivo data. This opens for alternative explanations of how locomotion activity patterns in the adult mammal could be generated. Author summaryLocomotion control in animals is hypothesized to be controlled through an intrinsic central pattern generator in the spinal cord. This was proposed over a hundred years ago and has subsequently been formed into a consistent theory, through experimentation and computer modeling. However, critical data that support the neuronal circuitry mechanisms underpinning this theory has been obtained in experiments that greatly differ from intact animals. We propose, after trying to fill in this critical part, that new ideas are required to explain locomotion of intact animals. 14 alternating oscillation in activity between the two half centers. The alternation would 15 ensure left right alternation and alternation between antagonists. This model would 16 explain locomotion in decerebrated animals [1], fictive locomotion [5] and locomotion 17 patterns in intact animals [6]. Neurophysiological evidence for a circuit fitting the half 18 center model was found [7] and subsequently substantiated by further findings [8-10]. 19The half center is a key component of computational and other models of the 20 CPG [5,6,[11][12][13][14]. Asymmetric half center models have been proposed to explain 21 alternation between flexor and extensor [15]. We focus on the symmetric case. 22Experimental studies show that reciprocal inhibition is necessary to ensure left right 23 alternation [16], hence reciprocal inhibition must be present in the CPG. 24However, it was already noted that two groups of neurons inhibiting each other are 25 not sufficient to generate oscillation [1,7]. We will formally demonstrate why this is the 26 case using a mean field model. Without a mechanism that stops neurons from indefinite 27 activity, one h...

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More conditioning stimuli enhance synaptic plasticity in the human spinal cord

Cited by 27 publications

References 35 publications

Induction of plasticity in the human motor system by motor imagery and transcranial magnetic stimulation

Induction of plasticity in the human motor system by motor imagery and transcranial magnetic stimulation

Transcutaneous spinal direct current stimulation increases corticospinal transmission and enhances voluntary motor output in humans

Biological data questions the support of the self inhibition required for pattern generation in the half center model

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