STUDY DESIGN: A weight-drop device based on a displacement transducer and feedback detection circuitry was designed to produce consistent experimental spinal cord injuries in a rat model. The device was characterized and evaluated based on biomechanical parameters, quantitative histology, and neurologic behavior. OBJECTIVE: To develop, characterize, and evaluate a spinal cord injury device for use in animal models. SUMMARY OF BACKGROUND DATA: The biomechanical parameters of spinal cord injury, including compression, velocity, force, energy, impulse-momentum, and power, can be derived from the displacement waveform. It has been shown that the magnitude and variability of certain of these injury parameters are correlated with lesion size and neurologic deficit. METHODS: Two groups of six male Sprague-Dawley rats were injured using the device and their injury displacement waveforms digitally recorded on a personal computer equipped with a data acquisition board. Group 1 animals were sacrificed immediately after injury, whereas Group 2 animals were sacrificed 14 days after injury. Quantitative morphometric and numerical analyses were performed on histologic specimens and injury waveforms, respectively. Biomechanical injury parameters were compared with histologic and behavioral measures of injury. RESULTS: All kinetic injury parameters were reproducible to within standard deviations of less than +/- 22%, whereas spinal cord displacement variability was +/- 29%. Motor scores for animals on day 14 animals were 4.3 +/- 0.4, whereas lesion sizes were much more variable, exhibiting percent volumes of 5.5 +/- 2.5 immediately after injury, and 11.9 +/- 7.1 on day 14. CONCLUSION: This device should benefit studies of experimental spinal cord injury in animals by reducing interanimal variations in injury severity, especially in the acute phase of injury.

Animals↗

PubMed1996

Diminished microtubule-associated protein 2 (MAP2) immunoreactivity following cortical impact brain injury.

This study employed Western blotting and qualitative immunohistochemistry to analyze the effects of cortical impact traumatic brain injury (TBI) on acute changes in MAP2 immunoreactivity in the rat cortex. We employed a lateral cortical impact injury device to induce severe TBI, which is associated with focal cortical contusion and neuronal death at the impact site. Three hours following TBI, Western blotting detected substantial MAP2 loss only in the cortex ipsilateral to the site of injury. Light microscopic studies of MAP2 revealed a prominent loss of MAP2 immunofluorescence in apical dendrites of pyramidal neurons within layers 3 and 5, as well as a loss of fine dendritic arborization within layer 1. These changes in MAP2 immunolabeling were associated with, but not exclusively restricted to, the presence of dark shrunken neurons labeled by hematoxylin and eosin staining, suggesting impending cell death. Alterations in MAP2 immunofluorescence were found both within and beyond areas of focal contusion and necrosis in the ipsilateral cortex. Thus, traumatic brain injury in rats can produce rapid and significant dendritic pathology within sites of contusion. However, immunohistochemical changes in MAP2 labeling outside of contused regions suggests that TBI-induced dendritic damage may not be exclusively associated with acute cell death.

Animals↗

PubMed1996