Enhanced Behavioral Recovery from Sensorimotor Cortex Lesions After Pyramidotomy in Adult Rats

Fanardjian, V.V.; Gevorkyan, O. V.; Mallina, Ravi; Melik-Moussian, A.B.; Meliksetyan, I. B.

doi:10.1155/np.2000.261

Cited by 9 publications

(7 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…24 Because the corticospinal and rubrospinal axons possess similar branching patterns in the spinal cord, 25 the corticorubrospinal pathway seems to be a backup to the CST to enhance the behavioral recovery after CST lesion. 26 We also found that GAP-43 immunostaining was increased in neurites other than CST axons in the spinal cord after stroke, suggesting a possibility that stroke-induced denervation also enhances axonal plasticity of non-CST pathways and increases the neurite arborization of the spinal neurons. Further studies are warranted to investigate neuronal plasticity in the spinal cord after stroke.…”

Section: Discussionsupporting

confidence: 50%

Axonal Remodeling of the Corticospinal Tract in the Spinal Cord Contributes to Voluntary Motor Recovery After Stroke in Adult Mice

Liu

Chopp²,

Ding³

et al. 2013

Stroke

View full text Add to dashboard Cite

Background and Purpose We sought to demonstrate the contribution of axonal remodeling of the corticospinal tract (CST) in the spinal cord to functional outcome after stroke. Methods Bilateral pyramidotomy (BPT) or sham-BPT was performed in mice with transgenic yellow fluorescent protein labeling in the CST subjected to middle cerebral artery occlusion (MCAo). Foot-fault and single pellet reaching tests were performed 3 days after MCAo and weekly thereafter. Mice were euthanized at day 14 or 28 after stroke. Immunofluorescent staining for growth-associated protein-43 and Synaptophysin was performed on cervical sections. Results Functional improvements were evident during the initial 14 days in both MCAo-sham-BPT and MCAo-BPT mice (P<0.01, versus day 3). Progressive recovery was present during the subsequent 14 days in MCAo-sham-BPT mice (P<0.001, versus day 14) but not in MCAo-BPT mice. In the stroke-affected cervical gray matter of MCAo-sham-BPT mice, growth-associated protein-43-Cy3 staining on CST axons were significantly increased at day 14 after stroke compared with normal mice (P<0.001), and CST axonal density and Synaptophysin-Cy3 staining of CST-yellow fluorescent protein axonal terminals were significantly increased at day 28 compared with day 14 after MCAo (P<0.001). Conclusions Our data demonstrate that voluntary motor recovery is associated with CST axonal outgrowth and synaptic formation in the denervated side of the spinal gray matter during the later phase after stroke, suggesting that the CST axonal plasticity in the spinal cord contributes to neurological recovery.

show abstract

Section: Discussionsupporting

confidence: 50%

Axonal Remodeling of the Corticospinal Tract in the Spinal Cord Contributes to Voluntary Motor Recovery After Stroke in Adult Mice

Liu

Chopp²,

Ding³

et al. 2013

Stroke

View full text Add to dashboard Cite

show abstract

“…However, the rubrospinal tract participates in the coordination of movements across joints, such as skilled forelimb movements [33], locomotion [34] and motor responses to pain [35], and possesses very similar branching patterns with the CST in the spinal cord [36]. The cortico-rubrospinal pathway appears to be a backup to the CST to enhance the behavioral recovery after CST lesion [37]. We and others have demonstrated that axonal plasticity of the corticorubral tract [38]–[40] and other spinal descending pathways [41] contribute to functional recovery after stroke in rodents.…”

Section: Discussionmentioning

confidence: 99%

Plasminogen Deficiency Causes Reduced Corticospinal Axonal Plasticity and Functional Recovery after Stroke in Mice

Liu

Qian

et al. 2014

PLoS ONE

View full text Add to dashboard Cite

Tissue plasminogen activator (tPA) has been implicated in neurite outgrowth and neurological recovery post stroke. tPA converts the zymogen plasminogen (Plg) into plasmin. In this study, using plasminogen knockout (Plg-/-) mice and their Plg-native littermates (Plg+/+), we investigated the role of Plg in axonal remodeling and neurological recovery after stroke. Plg+/+ and Plg-/- mice (n = 10/group) were subjected to permanent intraluminal monofilament middle cerebral artery occlusion (MCAo). A foot-fault test and a single pellet reaching test were performed prior to and on day 3 after stroke, and weekly thereafter to monitor functional deficit and recovery. Biotinylated dextran amine (BDA) was injected into the left motor cortex to anterogradely label the corticospinal tract (CST). Animals were euthanized 4 weeks after stroke. Neurite outgrowth was also measured in primary cultured cortical neurons harvested from Plg+/+ and Plg-/- embryos. In Plg+/+ mice, the motor functional deficiency after stroke progressively recovered with time. In contrast, recovery in Plg-/- mice was significantly impaired compared to Plg+/+ mice (p<0.01). BDA-positive axonal density of the CST originating from the contralesional cortex in the denervated side of the cervical gray matter was significantly reduced in Plg-/- mice compared with Plg+/+ mice (p<0.05). The behavioral outcome was highly correlated with the midline-crossing CST axonal density (R2>0.82, p<0.01). Plg-/- neurons exhibited significantly reduced neurite outgrowth. Our data suggest that plasminogen-dependent proteolysis has a beneficial effect during neurological recovery after stroke, at least in part, by promoting axonal remodeling in the denervated spinal cord.

show abstract

“…Third, descending inputs other than the fast corticospinal elements are used 245. Numerous animal studies involving experimental sensorimotor cortex or spinal cord lesions support the hypothesis that motor recovery involves switching of motor activity to the control of brainstem descending pathways such as the cortico‐rubrospinal, the cortico‐reticulospinal, and the cortico‐vestibulospinal systems 15, 48, 72, 191, 192, 250, 274. Propriospinal neurons may also be involved in strategies for functional recovery.…”

Section: Immediate Effects Of Central Lesionmentioning

confidence: 99%

Pathophysiology of spastic paresis. I: Paresis and soft tissue changes

2005

View full text Add to dashboard Cite

Spastic paresis follows chronic disruption of the central execution of volitional command. Motor function in patients with spastic paresis is subjected over time to three fundamental insults, of which the last two are avoidable: (1) the neural insult itself, which causes paresis, i.e., reduced voluntary motor unit recruitment; (2) the relative immobilization of the paretic body part, commonly imposed by the current care environment, which causes adaptive shortening of the muscles left in a shortened position and joint contracture; and (3) the chronic disuse of the paretic body part, which is typically self-imposed in most patients. Chronic disuse causes plastic rearrangements in the higher centers that further reduce the ability to voluntarily recruit motor units, i.e., that aggravate baseline paresis. Part I of this review focuses on the pathophysiology of the first two factors causing motor impairment in spastic paresis: the vicious cycle of paresis-disuse-paresis and the contracture in soft tissues.

show abstract

Enhanced Behavioral Recovery from Sensorimotor Cortex Lesions After Pyramidotomy in Adult Rats

Cited by 9 publications

References 45 publications

Axonal Remodeling of the Corticospinal Tract in the Spinal Cord Contributes to Voluntary Motor Recovery After Stroke in Adult Mice

Axonal Remodeling of the Corticospinal Tract in the Spinal Cord Contributes to Voluntary Motor Recovery After Stroke in Adult Mice

Plasminogen Deficiency Causes Reduced Corticospinal Axonal Plasticity and Functional Recovery after Stroke in Mice

Pathophysiology of spastic paresis. I: Paresis and soft tissue changes

Contact Info

Product

Resources

About