Reorganization of movement representations in primary motor cortex following focal ischemic infarcts in adult squirrel monkeys

Nudo, RJ; Milliken, Garrett W.

doi:10.1152/jn.1996.75.5.2144

Cited by 706 publications

(485 citation statements)

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“…Reorganicombined use of drug therapy together with the physical zation of motor cortex after lesioning can occur, as therapy. Pharmacological intervention can alter plastic demonstrated by Nudo and colleagues [49,50] in the changes. The best documented influence is with amphetprimate, but this appears to require attempted use of the amine and related noradrenergic agents [21,22].…”

Section: Mechanisms Of Plasticitymentioning

confidence: 99%

Plasticity of the human motor cortex and recovery from stroke

Hallett

2001

Brain Research Reviews

316

178

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By a variety of mechanisms, the human brain is constantly undergoing plastic changes. Plasticity can be studied with phenomena such as peripheral deafferentation and motor learning. Spontaneous recovery from stroke in the chronic stage likely comes about because of plasticity, and the best recovery seems to result from reorganization in the damaged hemisphere. Knowledge about the physiology of brain plasticity has led to the development of new techniques for rehabilitation. Published by Elsevier Science B. V. Theme: Development and regenerationTopic: Motor systems

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Section: Mechanisms Of Plasticitymentioning

confidence: 99%

Plasticity of the human motor cortex and recovery from stroke

Hallett

2001

Brain Research Reviews

316

178

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“…Functional imaging of stroke patients (Chollet et al, 1991;Ward et al, 2003aWard et al, ,b, 2006Fridman et al, 2004;Jaillard et al, 2005;Rossini et al, 2007) and intracranial microstimulation (ICMS) studies in animal models (Castro-Alamancos and Borrel, 1995;Nudo and Milliken, 1996;Friel et al, 2000;Frost et al, 2003;Kleim et al, 2003;Gharbawie et al, 2005) suggest that surviving cortex can adopt the motor or sensory processing functions of regions lost to damage. Functional imaging and ICMS are powerful tools for assessing regional plasticity, but lack the spatial and temporal resolution to define how activity in single neurons or local neuronal ensembles are changing relative to infarct boundaries.…”

Section: Introductionmentioning

confidence: 99%

In Vivo Calcium Imaging Reveals Functional Rewiring of Single Somatosensory Neurons after Stroke

Winship¹,

Murphy²

2008

Journal of Neuroscience

161

182

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Functional mapping and microstimulation studies suggest that recovery after stroke damage can be attributed to surviving brain regions taking on the functional roles of lost tissues. Although this model is well supported by data, it is not clear how activity in single neurons is altered in relation to cortical functional maps. It is conceivable that individual surviving neurons could adopt new roles at the expense of their usual function. Alternatively, neurons that contribute to recovery may take on multiple functions and exhibit a wider repertoire of neuronal processing. In vivo two-photon calcium imaging was used in adult mice within reorganized forelimb and hindlimb somatosensory functional maps to determine how the response properties of individual neurons and glia were altered during recovery from ischemic damage over a period of 2-8 weeks. Single-cell calcium imaging revealed that the limb selectivity of individual neurons was altered during recovery from ischemia, such that neurons normally selective for a single contralateral limb processed information from multiple limbs. Altered limb selectivity was most prominent in border regions between stroke-altered forelimb and hindlimb macroscopic map representations, and peaked 1 month after the targeted insult. Two months after stroke, individual neurons near the center of reorganized functional areas became more selective for a preferred limb. These previously unreported forms of plasticity indicate that in adult animals, seemingly hardwired cortical neurons first adopt wider functional roles as they develop strategies to compensate for loss of specific sensory modalities after forms of brain damage such as stroke.

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“…We used a model system to study the cellular mechanisms of synaptic remodeling following axon injury; this model recapitulated several hallmarks of neurons subjected to axonal injury in vivo, including chromatolysis 6,21 , retrograde spine loss 4,22,23 , retrograde hyper-excitability [1][2][3] , and disinhibition 2, 9, 10 . Axotomy-induced transcriptional changes in this in vitro model are also consistent with in vivo findings 7,20 .…”

Section: Discussionmentioning

confidence: 99%

“…A cquired brain injuries, such as occur in stroke and traumatic brain injury, induce significant synaptic reorganization, even in uninjured cortical regions remote from the site of damage [1][2][3] . This enhanced neural plasticity supports formation of new connections and expansion of cortical territories, well-described in humans using neuroimaging and non-invasive stimulation techniques 1,2,4,5 .…”

mentioning

confidence: 99%

Distal axotomy enhances retrograde presynaptic excitability onto injured pyramidal neurons via trans-synaptic signaling

Nagendran

Larsen

Bigler

et al. 2016

Preprint

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Injury of CNS nerve tracts remodels circuitry through dendritic spine loss and hyper-excitability, thus influencing recovery. Due to the complexity of the CNS, a mechanistic understanding of injury-induced synaptic remodeling remains unclear. Using microfluidic chambers to separate and injure distal axons, we show that axotomy causes retrograde dendritic spine loss at directly injured pyramidal neurons followed by retrograde presynaptic hyper-excitability. These remodeling events require activity at the site of injury, axon-to-soma signaling, and transcription. Similarly, directly injured corticospinal neurons in vivo also exhibit a specific increase in spiking following axon injury. Axotomy-induced hyperexcitability of cultured neurons coincides with elimination of inhibitory inputs onto injured neurons, including those formed onto dendritic spines. Netrin-1 downregulation occurs following axon injury and exogenous netrin-1 applied after injury normalizes spine density, presynaptic excitability, and inhibitory inputs at injured neurons. Our findings show that intrinsic signaling within damaged neurons regulates synaptic remodeling and involves netrin-1 signaling.

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Reorganization of movement representations in primary motor cortex following focal ischemic infarcts in adult squirrel monkeys

Cited by 706 publications

References 0 publications

Plasticity of the human motor cortex and recovery from stroke

Plasticity of the human motor cortex and recovery from stroke

In Vivo Calcium Imaging Reveals Functional Rewiring of Single Somatosensory Neurons after Stroke

Distal axotomy enhances retrograde presynaptic excitability onto injured pyramidal neurons via trans-synaptic signaling

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