X-irradiation of the Contusion Site Improves Locomotor and Histological Outcomes in Spinal Cord-Injured Rats

Zeman, Richard J.; Feng, Yong; Peng, Hong; Visintainer, Paul; Couldwell, William T.; Etlinger, Joseph D.

doi:10.1006/exnr.2001.7803

Cited by 31 publications

(29 citation statements)

References 24 publications

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“…A consistent feature of studies using the contusion model of spinal cord injury is that the magnitude of locomotor recovery is closely paralleled by the extent of tissue sparing at the contusion epicenter over a range of injury severities (Basso et al, 1996;Noble and Wrathall, 1985;Zeman et al, 1999Zeman et al, , 2001. Consistent with this, in the present experiments, improved locomotor recovery by tempol was also associated with sparing of spinal cord tissue at the epicenter.…”

Section: Discussionsupporting

confidence: 85%

“…As in our previous studies (Zeman et al, 1999(Zeman et al, , 2001, the spinal cords were contused with a weight-drop apparatus similar to the NYU impactor (Basso et al, 1996;Gruner, 1992) at the level of T10. Prior to surgery, the rats were anesthetized with an injection of pentobarbital sodium (60 mg/kg ip), and laminectomy was performed aseptically at T9-T10 to expose the spinal cord.…”

Section: Methodsmentioning

confidence: 99%

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Tempol, a Nitroxide Antioxidant, Improves Locomotor and Histological Outcomes after Spinal Cord Contusion in Rats

Hillard

Peng

Zhang

et al. 2004

Journal of Neurotrauma

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We have determined whether the nitroxide antioxidant, tempol, can oppose tissue loss and improve recovery of locomotor function following contusion injury of the spinal cord. Contusion injury was produced in rats at the level of T10 with a weight-drop device and locomotor recovery was determined with the 21-point Basso, Beattie and Bresnahan (BBB) scale. Locomotor function recovered progressively during the 6-week postinjury observation period and was significantly greater in tempol-treated (275 mg/kg i.p., 20 min postinjury) compared to vehicle-treated rats (final BBB scores: 9.1 versus 6.4). Similarly enhanced locomotor recovery was observed with doses of tempol in the range of 138-550, but not 69 mg/kg, and with injection at 48 h postinjury indicating a therapeutic time-window of at least several days. The extent of recovery correlated with measurements of sparing of spinal cord white matter in a region several millimeters in length extending rostrally from the contusion epicenter. In contrast, loss of gray matter was unaffected by tempol treatment. Since tempol acts by scavenging reactive oxygen species (ROS) such as superoxide and hydroxyl radicals, the improved locomotor recovery and spared spinal cord tissue following contusion injury provides evidence of a direct role of ROS-mediated neurodegeneration in spinal cord injury.

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Section: Discussionsupporting

confidence: 85%

Section: Methodsmentioning

confidence: 99%

Tempol, a Nitroxide Antioxidant, Improves Locomotor and Histological Outcomes after Spinal Cord Contusion in Rats

Hillard

Peng

Zhang

et al. 2004

Journal of Neurotrauma

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“…There are several promising neuroregenerative and neuroprotective treatments that are directed to limit neuronal damage and/or induce neuronal regeneration after a spinal cord injury (SCI) [1][2][3] and they will enter the clinic within the next decade. [4][5][6] However, the auspicious results in animal experiments often cannot be replicated in humans.…”

Section: Introductionmentioning

confidence: 99%

Neuronal dysfunction in chronic spinal cord injury

2010

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This review describes the changes of spinal neuronal function that occur after a motor complete spinal cord injury (cSCI) in humans. In healthy subjects, polysynaptic spinal reflex (SR) evoked by non-noxious tibial nerve stimulation consists of an early SR component and rarely a late SR component. Soon after a cSCI, SR and locomotor activity are absent. After spinal shock; however, an early SR component re-appears associated with the recovery of locomotor activity in response to appropriate peripheral afferent input. Clinical signs of spasticity take place in the following months, largely as a result of nonneuronal changes. After around 1 year, the locomotor and SR activity undergo fundamental changes, that is, the electromyographic amplitude in the leg muscles during assisted locomotion exhaust rapidly, accompanied by a shift from early to dominant late SR components. The exhaustion of locomotor activity is also observed in non-ambulatory patients with an incomplete spinal cord injury (SCI). At about 1 year after injury, in most cSCI subjects the neuronal dysfunction is fully established and remains more or less stable in the following years. It is assumed that in chronic SCI, the patient's immobility resulting in a reduced input from supraspinal and peripheral sources leads to a predominance of inhibitory drive within spinal neuronal circuitries underlying locomotor pattern and SR generation. Training of spinal interneuronal circuits including the enhancement of an appropriate afferent input might serve as an intervention to prevent neuronal dysfunction after an SCI.

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“…Therefore, inhibition of the over-proliferation of either reactive astrocytes or fi broblasts after CNS injury may signifi cantly reduce the scarring. Previous research reported that an optimal dose of X-irradiation eliminates connective tissue scars as well as glial scars in a rat model of SCI [59,60] . More physical interventions targeting scar formation after SCI have been described in a previous review [61] .…”

Section: Inhibition Of Fibrotic Scar Formationmentioning

confidence: 99%