Experimental neurology
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Experimental neurology · Jan 2000
Light and confocal microscopic studies of evolutionary changes in neurofilament proteins following cortical impact injury in the rat.
Previous studies have shown that traumatic brain injury (TBI) produces progressive degradation of cytoskeletal proteins including neurofilaments (e.g., neurofilament 68 [NF68] and neurofilament 200 [NF200]) within the first 24 h after injury. Thus, we employed immunofluorescence (light and confocal microscopy) to study the histopathological correlates of progressive neurofilament protein loss observed at 15 min, 3 h, and 24 h following unilateral cortical injury in rats. TBI produced significant alterations in NF68 and NF200 immunolabeling in dendrites and cell bodies at contusion sites ipsilateral to injury, as well as in the noncontused contralateral cortex. ⋯ Moreover, changes in dendritic cytoskeletal proteins are progressive and not fully expressed within the first 15 min following impact injury. These progressive dendritic disruptions are characterized by disturbances in the morphology of neurofilament proteins, resulting in fragmentation and focal loss of NF68 immunofluorescence within apical dendrites. In contrast, alterations in axonal cytoskeletal proteins are more restricted and delayed with no pronounced changes until 24 h after injury.
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Experimental neurology · Jan 2000
Effects of spinal cord X-irradiation on the recovery of paraplegic rats.
Axonal regrowth is limited in the adult CNS, especially in the spinal cord, one of the major sites of traumatic lesions. Pathophysiological changes occurring after spinal cord injury include complex acute, subacute, and late processes. In this study, we assessed whether X-irradiation interferes with the acute/subacute phases, thereby improving the functional recovery of paraplegic animals. ⋯ There was a 23% less lesion-induced syringomyelia in the 2-Gy group than in the other groups (LNI and 5-20 Gy). Thus, low doses of X-rays may interfere with the formation of syringomyelia and glial scar, thereby facilitating the recovery of paraplegic animals. These findings suggest that low-dose irradiation of the lesion site, in association with other therapies, is a potentially promising treatment for improving recovery after spinal cord injury.
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Experimental neurology · Jan 2000
Sciatic nerve transection in the adult rat: abnormal EMG patterns during locomotion by aberrant innervation of hindleg muscles.
The effects of lesions in the sciatic nerve were studied in adult rats. In the left hindleg, a segment 12 mm long was resected from the proximal part of the nerve, before the bifurcation into the peroneal and tibial nerves. This segment in a reversed orientation was used as a nerve graft. ⋯ Neuronal diameters were slightly decreased but a considerable decrease was observed in dendritic branching and dendrite bundles in the pools of the SOL and in the GC were absent. No consistent trends in neuronal numbers at the affected side in comparison to the right side were detected. We conclude that axons, sprouting from the proximal stump of the sciatic nerve, innervate the muscles aselectively and that the motoneurons of origin maintain their original activation pattern.
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Experimental neurology · Jan 2000
Neuronal subclass-selective loss of pyruvate dehydrogenase immunoreactivity following canine cardiac arrest and resuscitation.
Chronic impairment of aerobic energy metabolism accompanies global cerebral ischemia and reperfusion and likely contributes to delayed neuronal cell death. Reperfusion-dependent inhibition of pyruvate dehydrogenase complex (PDHC) enzyme activity has been described and proposed to be at least partially responsible for this metabolic abnormality. This study tested the hypothesis that global cerebral ischemia and reperfusion results in the loss of pyruvate dehydrogenase immunoreactivity and that such loss is associated with selective neuronal vulnerability to transient ischemia. ⋯ A significant decrease in immunoreactivity was observed in frontal cortex homogenates from both 2 and 24 h reperfused animals compared to samples from nonischemic control animals. These results were supported by confocal microscopic immunohistochemical determinations of pyruvate dehydrogenase immunoreactivity in the neuronal cell bodies located within different layers of the frontal cortex. Loss of immunoreactivity was greatest for pyramidal neurons located in layer V compared to neurons in layers IIIc/IV, which correlates with a greater vulnerability of layer V neurons to delayed death caused by transient global cerebral ischemia.