Motoneuron Intrinsic Properties, but Not Their Receptive Fields, Recover in Chronic Spinal Injury

Johnson, Michael D.; Kajtaz, Elma; Cain, Charlette M.; Heckman, C. J.

doi:10.1523/jneurosci.2609-13.2013

Cited by 20 publications

(23 citation statements)

References 57 publications

(15 reference statements)

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“…Moreover, the time course of the MN Kv2.1 channel response is likewise consistent with observations that intrinsic homeostatic mechanisms can respond more rapidly than synaptic mechanisms (Karmarkar and Buonomano 2006). Many electrophysiological and modeling studies show that MN intrinsic properties respond profoundly to both pathologic and nonpathologic alterations in activity (Kuno et al 1974a,b;Gustafsson and Pinter 1984;Foehring et al 1986a,b;Wolpaw and Tennissen 2001;Bichler et al 2007a;Meehan et al 2010;Prather et al 2011;Quinlan et al 2011;Johnson et al 2013). However, only a few motoneuron studies have characterized the ion channel alterations that could underlie these effects, and of these studies, most examined transcriptional expression changes over days to weeks (Anneser et al 1999(Anneser et al , 2000Alvarez and Fyffe 2007;Woodrow et al 2013).…”

Section: An Intrinsic Neuronal Mechanism For Homeostatic Plasticitysupporting

confidence: 72%

“…; Johnson et al. ). However, only a few motoneuron studies have characterized the ion channel alterations that could underlie these effects, and of these studies, most examined transcriptional expression changes over days to weeks (Anneser et al.…”

Section: Discussionmentioning

confidence: 97%

“…; Johnson et al. ). Identifying the responsible conductances and related ion channel expression patterns is critical to understanding MN physiology and pathology.…”

Section: Introductionmentioning

confidence: 97%

“…The localization of ion channels within certain membrane compartments and/or signaling ensembles is critical to synaptic integration and shaping of firing properties (Deardorff et al 2013Romer et al 2014). In spinal motoneurons (MNs), as in other cell types, intrinsic membrane properties can be dynamically modified by changes in neuronal activity and pathology (Kuno et al 1974a,b;Gustafsson and Pinter 1984;Foehring et al 1986a,b;Wolpaw and Tennissen 2001;Bichler et al 2007a; Meehan et al 2010;Prather et al 2011;Quinlan et al 2011;Johnson et al 2013). Identifying the responsible conductances and related ion channel expression patterns is critical to understanding MN physiology and pathology.…”

Section: Introductionmentioning

confidence: 99%

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Activity-dependent redistribution of Kv2.1 ion channels on rat spinal motoneurons

2016

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Homeostatic plasticity occurs through diverse cellular and synaptic mechanisms, and extensive investigations over the preceding decade have established Kv2.1 ion channels as key homeostatic regulatory elements in several central neuronal systems. As in these cellular systems, Kv2.1 channels in spinal motoneurons (MNs) localize within large somatic membrane clusters. However, their role in regulating motoneuron activity is not fully established in vivo. We have previously demonstrated marked Kv2.1 channel redistribution in MNs following in vitro glutamate application and in vivo peripheral nerve injury (Romer et al., 2014, Brain Research, 1547:1–15). Here, we extend these findings through the novel use of a fully intact, in vivo rat preparation to show that Kv2.1 ion channels in lumbar MNs rapidly and reversibly redistribute throughout the somatic membrane following 10 min of electrophysiological sensory and/or motor nerve stimulation. These data establish that Kv2.1 channels are remarkably responsive in vivo to electrically evoked and synaptically driven action potentials in MNs, and strongly implicate motoneuron Kv2.1 channels in the rapid homeostatic response to altered neuronal activity.

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Section: An Intrinsic Neuronal Mechanism For Homeostatic Plasticitysupporting

confidence: 72%

Section: Discussionmentioning

confidence: 97%

“…; Johnson et al. ). Identifying the responsible conductances and related ion channel expression patterns is critical to understanding MN physiology and pathology.…”

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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Activity-dependent redistribution of Kv2.1 ion channels on rat spinal motoneurons

2016

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“…100,101 In addition, although PICs are recovered following SCI in cats, the movement-related receptive fields (MRRF) are no longer joint-specific: ankle extensor motoneurons are not only activated by passive ankle rotations but also by rotations of the hip. 102,103 The injury-related widening of the MRRF is most likely due to the loss of monoaminergic modulation causing a disinhibition of polysynaptic excitatory pathways on target motoneurons, which has the potential to activate muscles through the entire limb and possibly contribute to spasms. 102 It also is important to note that although a complete spinal cord transection typically is not considered the most clinically relevant model, these animals display more spasticity than contused animals, 104 unlike SCI individuals who show more spasticity with moderate injuries.…”

Section: Motoneurons As a Target For Locomotor Training: A Balancing mentioning

confidence: 99%

Rehabilitation Strategies after Spinal Cord Injury: Inquiry into the Mechanisms of Success and Failure

Côté

Murray

Lemay

2017

Journal of Neurotrauma

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Body-weight supported locomotor training (BWST) promotes recovery of load-bearing stepping in lower mammals, but its efficacy in individuals with a spinal cord injury (SCI) is limited and highly dependent on injury severity. While animal models with complete spinal transections recover stepping with step-training, motor complete SCI individuals do not, despite similarly intensive training. In this review, we examine the significant differences between humans and animal models that may explain this discrepancy in the results obtained with BWST. We also summarize the known effects of SCI and locomotor training on the muscular, motoneuronal, interneuronal, and supraspinal systems in human and non-human models of SCI and address the potential causes for failure to translate to the clinic. The evidence points to a deficiency in neuronal activation as the mechanism of failure, rather than muscular insufficiency. While motoneuronal and interneuronal systems cannot be directly probed in humans, the changes brought upon by step-training in SCI animal models suggest a beneficial re-organization of the systems' responsiveness to descending and afferent feedback that support locomotor recovery. The literature on partial lesions in humans and animal models clearly demonstrate a greater dependency on supraspinal input to the lumbar cord in humans than in non-human mammals for locomotion. Recent results with epidural stimulation that activates the lumbar interneuronal networks and/or increases the overall excitability of the locomotor centers suggest that these centers are much more dependent on the supraspinal tonic drive in humans. Sensory feedback shapes the locomotor output in animal models but does not appear to be sufficient to drive it in humans.

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Redistribution of inhibitory force feedback between a long toe flexor and the major ankle extensor muscles following spinal cord injury

Niazi

Lyle

Rising

et al. 2020

J of Neuroscience Research

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Inhibitory pathways from Golgi tendon organs project widely between muscles crossing different joints and axes of rotation. Evidence suggests that the strength and distribution of this intermuscular inhibition is dependent on motor task and corresponding signals from the brainstem. The purpose of the present study was to investigate whether this sensory network is altered after spinal cord hemisection as a potential explanation for motor deficits observed after spinal cord injury (SCI). Force feedback was assessed between the long toe flexor and ankle plantarflexor (flexor hallucis longus), and the three major ankle extensors, (combined gastrocnemius, soleus, and plantaris muscles) in the hind limbs of unanesthetized, decerebrate, female cats. Data were collected from animals with intact spinal cords (control) and lateral spinal hemisections (LSHs) including chronic LSH (4–20 weeks), subchronic LSH (2 weeks), and acute LSH. Muscles were stretched individually and in pairwise combinations to measure intermuscular feedback between the toe flexor and each of the ankle extensors. In control animals, three patterns were observed (balanced inhibition between toe flexor and ankle extensors, stronger inhibition from toe flexor to ankle extensor, and vice versa). Following spinal hemisection, only strong inhibition from toe flexors onto ankle extensors was observed independent of survival time. The results suggest immediate and permanent reorganization of force feedback in the injured spinal cord. The altered strength and distribution of force feedback after SCI may be an important future target for rehabilitation.

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Motoneuron Intrinsic Properties, but Not Their Receptive Fields, Recover in Chronic Spinal Injury

Cited by 20 publications

References 57 publications

Activity-dependent redistribution of Kv2.1 ion channels on rat spinal motoneurons

Activity-dependent redistribution of Kv2.1 ion channels on rat spinal motoneurons

Rehabilitation Strategies after Spinal Cord Injury: Inquiry into the Mechanisms of Success and Failure

Redistribution of inhibitory force feedback between a long toe flexor and the major ankle extensor muscles following spinal cord injury

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