scholarly journals Effects of skilled and unskilled training on functional recovery and brain plasticity after focal ischemia in adult rats

2012 ◽  
Vol 1486 ◽  
pp. 53-61 ◽  
Author(s):  
A.S. Pagnussat ◽  
F. Simao ◽  
J.R. Anastacio ◽  
R.G. Mestriner ◽  
S.M. Michaelsen ◽  
...  
Keyword(s):  
Functional Recovery ◽  
Brain Plasticity ◽  
Focal Ischemia ◽  
Adult Rats

Abstract 3126: Ischemic Postconditioning Facilitates Brain Recovery After Stroke by Promoting mTOR Activity

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Peng Wang ◽  
Rong Xie ◽  
Xunming Ji ◽  
Heng Zhao
Keyword(s):  
Western Blotting ◽  
Brain Plasticity ◽  
Focal Ischemia ◽  
Mtor Pathway ◽  
Synaptic Function ◽  
Ischemic Postconditioning ◽  
Protein Levels ◽  
Left Lateral Ventricle ◽  
Brain Recovery ◽  
Mtor Activity

Introduction: Ischemic postconditioning represents a series of brief occlusions of blood flow before complete restoration of reperfusion after brain stroke. We have shown that ischemic postconditioning reduces infarct size in focal ischemia in rats and improves neurological deficits, but the underlying protective mechanisms are not fully understood. The mammalian target of rapamycin (mTOR) pathway plays a key role in cell growth, differentiation and survival. We studied the hypothesis that the mTOR pathway is involved in the protective effect of ischemic postconditioning and brain recovery after stroke in rats. Methods: Focal ischemia was induced by 30 min of bilateral CCA occlusion and permanent distal MCA occlusion in rats. Ischemic postconditioning was induced by 3 cycles of 30 sec reperfusion and 10 sec occlusion at the end of stroke. Rapamycin, an mTOR inhibitor, was injected into the left lateral ventricle 1 hour before stroke onset. For the behavior test, home cage and vibrissa-elicited limb use tests were used and performed until 21d after stroke. Peri-infarct tissues were collected 1 and 3 weeks after stroke for Western blotting and immunostaining. Molecular markers related with synaptic transmission and neuronal growth and plasticity, including Gap-43, synaptophysin, MAP-2 and PSD-95 proteins were detected. Protein levels of phosphorylated mTOR (p-MTOR) and 4EPB-1 in the mTOR pathway, and the upstream molecule, Akt, were also measured. Results: Ischemic postconditioning improved neurological function when measured 2 weeks after stroke (n=6, p<0.05), and reduced brain injury size by 34.2% (P<0.05). These protective effects were abolished by rapamycin treatment. The results of Western blotting showed that postconditioning substantially promoted the protein level of Gap-43, MAP-2 and PSD-95, but not synaptophysin. Rapamycin significantly inhibited Gap-43 levels at 1 and 3 weeks after stroke, and inhibited Map-2 level at 1 week (P<0.05). Postconditioning significantly increased the protein levels of p-Akt, p-mTOR, p-4EBP-1 compared with control ischemia (p<0.05) at 1 week after stroke injury. Rapamycin attenuated p-mTOR levels 1 and 3 weeks after stroke, and inhibited p-4EBP-1 level at 1 week (p<0.05), but had no effects on the expression level of p-Akt and Akt. Conclusion: Ischemic postconditioning improved brain function, which is consistent with the improved expression of proteins related with synaptic function and brain plasticity. This protection appears to be achieved by the enhanced mTOR activity.

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

Survival, regeneration and functional recovery of motoneurons in adult rats by reimplantation of ventral root following spinal root avulsion

2004 ◽  
Vol 19 (8) ◽  
pp. 2123-2131 ◽  
Author(s):  
Huai-Yu Gu ◽  
Hong Chai ◽  
Jian-Yi Zhang ◽  
Zhi-Bin Yao ◽  
Li-Hua Zhou ◽  
...  
Keyword(s):  
Functional Recovery ◽  
Ventral Root ◽  
Root Avulsion ◽  
Spinal Root ◽  
Adult Rats

DNA vaccine against NgR promotes functional recovery after spinal cord injury in adult rats

2007 ◽  
Vol 1147 ◽  
pp. 66-76 ◽  
Author(s):  
Panpan Yu ◽  
Lidong Huang ◽  
Jian Zou ◽  
Huiqing Zhu ◽  
Xiaofei Wang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Dna Vaccine ◽  
Functional Recovery ◽  
Adult Rats ◽  
Cord Injury

Abstract TP96: Functional Recovery and White Matter Repair After Exosomes Administration in Different Experimental Animal Models of Stroke

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Laura Otero Ortega ◽  
María Gutiérrez Fernández ◽  
Berta Rodríguez Frutos ◽  
Jaime Ramos Cejudo ◽  
Irene Lorenzo Llorente ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
White Matter ◽  
Functional Recovery ◽  
Brain Plasticity ◽  
Trophic Factors ◽  
Lesion Volume ◽  
Axonal Sprouting ◽  
Control Groups ◽  
Myelin Formation ◽  
White Matter Repair

Introduction: Extracellular vesicles such as exosomes has opened a new field of research. Exosomes are able to transfer DNAs, mRNAs, microRNAs, non-coding RNAs, proteins, trophic factors and lipids associated with brain plasticity enhancement after stroke. Aim: To investigate white matter repair after exosomes administration in two experimental models of subcortical stroke: ischemic and hemorrhage. Material/Methods: Subcortical ischemic stroke was induced by Endothelin-1 and Collagenase IV was used to induce subcortical hemorrhagic stroke into striatum. Intravenous exosomes or saline only were administrated at 24h after cerebral infarct as treatment. Exosomes were isolated from culture of adipose mesenchymal stem cell and they were characterized by Nanoshight, Electronic microscope, Western blot and Immunofluorescence. Proteins contained into exosomes were analyzed by Orbitrab. We analyzed functional recovery by Rotarod, beam walking and Rogers tests. Lesion volume and tract connectivity were studied by magnetic resonance image. Anterograde and retrograde tracers were used to analyze axonal sprouting. Myelin formation was analyzed by cryomielin. Results: Proteomics analysis of exosomes identified more than 1400 proteins, many of them involved in intercellular communication. DiI labeled-Exosomes were detected in brain and peripheral organs (liver, lung and spleen). After 28 days, treated groups showed smaller functional deficit compared to control groups in both hemorrhagic and ischemic models. Moreover, treated group showed an increase in tract connectivity at 7 and 28 days compared to control groups. Also, animals which received exosomes showed an increase axonal sprouting and myelin formation at 28 days after stroke in both hemorrhagic and ischemic stroke. The treated groups also showed higher levels of white matter-associated markers in the injured area than the control groups. Conclusion: White matter integrity in different subcortical strokes is in part restored by exosomes treatment, probably mediated by repair molecular factors implicated in axonal sprouting, remyelination and oligodendrogenesis. These findings are associated with improved functional recovery in both kinds of strokes.

Effects of sexual behavioral manipulation on brain plasticity in adult rats

1998 ◽  
Vol 47 (4) ◽  
pp. 349-355 ◽  
Author(s):  
Karianne N. Prince ◽  
Jeffrey S. Prince ◽  
Edward W. Kinghorn ◽  
Donovan E. Fleming ◽  
Reuben W. Rhees
Keyword(s):  
Brain Plasticity ◽  
Adult Rats ◽  
Behavioral Manipulation

DHAM-BMSC Matrix Promotes Axonal Regeneration and Functional Recovery After Spinal Cord Injury in Adult Rats

2009 ◽  
pp. 110306202455053
Author(s):  
Hongsheng Liang ◽  
Peng Liang ◽  
Ye Xu ◽  
Jianing Wu ◽  
Tao Liang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Functional Recovery ◽  
Axonal Regeneration ◽  
Adult Rats ◽  
Cord Injury

scholarly journals Celecoxib Induces Functional Recovery after Intracerebral Hemorrhage with Reduction of Brain Edema and Perihematomal Cell Death

2004 ◽  
Vol 24 (8) ◽  
pp. 926-933 ◽  
Author(s):  
Kon Chu ◽  
Sang-Wuk Jeong ◽  
Keun-Hwa Jung ◽  
So-Young Han ◽  
Soon-Tae Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Intracerebral Hemorrhage ◽  
Brain Edema ◽  
Functional Recovery ◽  
Autologous Blood ◽  
Prostaglandin E ◽  
Dependent Manner ◽  
Behavioral Tests ◽  
Adult Rats ◽  
Cox 2

The selective cyclooxygenase-2 (COX-2) inhibitor has been reported to have antiinflammatory, neuroprotective, and antioxidant effects in ischemia models. In this study, the authors examined whether a selective COX-2 inhibitor (celecoxib) reduces cerebral inflammation and edema after intracerebral hemorrhage (ICH), and whether functional recovery is sustained with longer treatment. ICH was induced using collagenase in adult rats. Celecoxib (10 or 20 mg/kg) was administered intraperitoneally 20 minutes, 6 hours, and 24 hours after ICH and then daily thereafter. Seventy-two hours after ICH induction, the rats were killed for histologic assessment and measurement of brain edema and prostaglandin E2. Behavioral tests were performed before and 1, 7, 14, 21, and 28 days after ICH. The brain water content of celecoxib-treated rats decreased both in lesioned and nonlesioned hemispheres in a dose-dependent manner. Compared with the ICH-only group, the number of TUNEL-positive, myeloperoxidase-positive, or OX42-positive cells was decreased in the periphery of hematoma and brain prostaglandin E2 level was reduced in the celecoxib-treated group. Celecoxib-treated rats recovered better by the behavioral tests at 7 days after ICH throughout the 28-day period, and the earlier the drug was administered, the better the functional recovery. Evidence of similar effects in an autologous blood–injected model showed that direct collagenase toxicity was not the major cause of inflammation or cell death. These data suggest that celecoxib treatment after ICH reduces prostaglandin E2 production, brain edema, inflammation, and perihematomal cell death in the perihematomal zone and induces better functional recovery.

scholarly journals Leukemia inhibitor factor promotes functional recovery and oligodendrocyte survival in rat models of focal ischemia

2014 ◽  
Vol 40 (7) ◽  
pp. 3111-3119 ◽  
Author(s):  
Derrick D. Rowe ◽  
Lisa A. Collier ◽  
Hilary A. Seifert ◽  
Cortney B. Chapman ◽  
Christopher C. Leonardo ◽  
...  
Keyword(s):  
Functional Recovery ◽  
Focal Ischemia ◽  
Rat Models ◽  
Leukemia Inhibitor Factor
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