Journal of neurotrauma
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Journal of neurotrauma · Dec 2010
Increased survival and reinnervation of cervical motoneurons by riluzole after avulsion of the C7 ventral root.
Although adult motoneurons do not die if their axons are injured at some distance from the cell body, they are unable to survive injury caused by ventral root avulsion. Some of the injured motoneurons can be rescued if the ventral root is re-inserted into the spinal cord. Brachial plexus injuries that involve the complete or partial avulsion of one or more cervical ventral roots can be treated successfully only if satisfactory numbers of motoneurons remain alive following such an injury at the time of reconstructive surgery. ⋯ Much greater numbers of axons regenerated when reimplantation was followed by riluzole treatment (573 ± 9 SEM). These results show that injured adult motoneurons can be rescued by riluzole treatment, even if they cannot regenerate their axons. Reinnervation of the peripheral targets can also be further improved with riluzole treatment.
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Journal of neurotrauma · Dec 2010
The hormone ghrelin prevents traumatic brain injury induced intestinal dysfunction.
Intestinal barrier breakdown following traumatic brain injury (TBI) is characterized by increased intestinal permeability, leading to bacterial translocation, and inflammation. The hormone ghrelin may prevent intestinal injury and have anti-inflammatory properties. We hypothesized that exogenous ghrelin prevents intestinal injury following TBI. ⋯ Ghrelin reduced TNF-α to sham levels (29.2 ± 5.0 pg/mL; p = NS). We therefore conclude that ghrelin prevents TBI-induced injury, as determined by intestinal permeability, histology, and intestinal levels of TNF-α. The mechanism for ghrelin mediating intestinal protection is likely multifactorial, and further studies are needed to delineate these possibilities.
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Journal of neurotrauma · Dec 2010
Pharyngeal selective brain cooling is associated with reduced CNS cortical lesion after experimental traumatic brain injury in rats.
Therapeutic hypothermia (TH) is still being explored as a therapeutic option after traumatic brain injury (TBI) but clinical data has not supported its efficacy. Experimental approaches were promising, but clinical data did not support its efficacy in the treatment of TBI. A novel approach of pharyngeal selective brain cooling (pSBC), recently introduced by our group, has been accompanied by superior neurofunctional, sensorimotor, and cognitive outcomes. ⋯ Animals that had undergone pSBC showed a significantly faster recovery of body weight starting on DPI 3, and had gained substantially more weight than TBI-only animals on DPI 14 (p < 0.001), indicating superior physical recovery. Areas of cortical damage were significantly smaller in pSBC animals compared to TBI-only animals (p < 0.01). pSBC was associated with preservation of cortical tissue ipsilateral to the lesion, and superior physical recovery after experimental TBI. These results complement earlier reports in which pSBC was associated with superior neurofunctional and cognitive outcomes using the same experimental model.
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Journal of neurotrauma · Dec 2010
Association of chronic vascular changes with functional outcome after traumatic brain injury in rats.
We tested the hypothesis that vascular remodeling in the cortex, hippocampus, and thalamus is associated with long-term functional recovery after traumatic brain injury (TBI). We induced TBI with lateral fluid-percussion (LFP) injury in adult rats. Animals were followed-up for 9 months, during which we tested motor performance using a neuroscore test, spatial learning and memory with a Morris water maze, and seizure susceptibility with a pentylenetetrazol (PTZ) test. ⋯ Chronic alterations in CBF could not be attributed to changes in vascular density. Association of thalamic hypervascularity to epileptogenesis warrants further studies. Finally, hippocampal hypoperfusion may predict later seizure susceptibility in the LFP injury model of TBI, which could be of value for pre-clinical antiepileptogenesis trials.
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Journal of neurotrauma · Dec 2010
Interferon-γ decreases chondroitin sulfate proteoglycan expression and enhances hindlimb function after spinal cord injury in mice.
Glial cells, including astrocytes and macrophages/microglia, are thought to modulate pathological states following spinal cord injury (SCI). In the present study, we evaluated the therapeutic effects of interferon-γ (IFN-γ), which is one of the cytokines regulating glial function, in a mouse contusive SCI model. We found that intraperitoneal injection of IFN-γ significantly facilitated locomotor improvement following SCI. ⋯ In addition, IFN-γ treatment enhanced the number of serotonin-positive nerve fibers and myelinated nerve fibers around the lesion epicenter. We also found that glial cell line-derived neurotrophic factor (GDNF) and insulin-like growth factor-1 (IGF-1) were upregulated post-SCI following IFN-γ treatment. Our results indicate that IFN-γ exhibits therapeutic effects in mouse contusive SCI, presumably by reducing CSPG expression from reactive astrocytes and increasing the expression of neurotrophic factors.