Neuropathology in sensory,but not motor,brainstem nuclei of the rat whisker circuit after diffuse brain injury |
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Authors: | Jahan D Miremami Pooja M Talauliker Jordan L Harrison |
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Institution: | 1. Department of Biology, College of Arts and Sciences, University of Kentucky College of Medicine
Lexington, KYUSA;2. Spinal Cord &3. Brain Injury Research Center, University of Kentucky College of Medicine
Lexington, KYUSA;4. Spinal Cord &5. Department of Anatomy &6. Neurobiology, University of Kentucky College of Medicine
Lexington, KYUSA;7. Department of Child Health, University of Arizona College of Medicine—Phoenix
Phoenix, AZUSA;8. BARROW Neurological Institute at Phoenix Children’s Hospital
Phoenix, AZUSA;9. Interdisciplinary Graduate Program in Neuroscience, Arizona State University
Tempe, AZUSA |
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Abstract: | Neurological dysfunction after traumatic brain injury (TBI) is associated with pathology in cortical, subcortical, and brainstem nuclei. Our laboratory has reported neuropathology and microglial activation in the somatosensory barrel cortex (S1BF) and ventral posterior medial thalamus (VPM) after diffuse TBI in the rat, which correlated with post-injury whisker sensory sensitivity. The present study extends our previous work by evaluating pathology in whisking-associated sensory and motor brainstem nuclei. Brains from adult, male rats were recovered over 1 month after midline fluid percussion or sham injury. The principal trigeminal nucleus (PrV, sensory nucleus) and facial nucleus (VIIN, motor nucleus) were examined for neuropathology (silver histochemistry) and microglial activation (Iba1). Significant neuropathology in PrV was evident at 2 and 7 days post-injury compared to sham. Iba1-labeled microglia showed swollen somata and thickened processes over 1 month post-injury. In contrast, the VIIN showed non-significant neuropathology and reduced labeling of activated Iba1 microglia over 1 month post-injury. Together with our previous data, neuropathology and neuroinflammation in the whisker somatosensory pathway may contribute to post-injury sensory sensitivity more than the motor pathway. Whether these findings are direct results of the mechanical injury or consequences of progressive degeneration remains to be determined. |
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Keywords: | Microglial activation neuropathology rat traumatic brain injury vibrissal circuitry |
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