Does time heal all wounds? Experimental diffuse traumatic brain injury results in persisting histopathology in the thalamus
| Autor: | Sarah B. Ogle, Theresa Currier Thomas, P. David Adelson, Hazel G. May, Benjamin M. Rumney, Jonathan Lifshitz |
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| Rok vydání: | 2018 |
| Předmět: |
Male
0301 basic medicine Silver Staining medicine.medical_specialty Pathology Time Factors Traumatic brain injury Thalamus Poison control Stimulation Sensory system Somatosensory system Article Rats Sprague-Dawley 03 medical and health sciences Behavioral Neuroscience Imaging Three-Dimensional 0302 clinical medicine Brain Injuries Traumatic medicine Animals Diffuse traumatic brain injury Neurons Neuronal Plasticity medicine.disease Immunohistochemistry Disease Models Animal 030104 developmental biology Astrocytes Acute Disease Chronic Disease Histopathology Microglia Psychology Neuroscience 030217 neurology & neurosurgery |
| Zdroj: | Behavioural Brain Research. 340:137-146 |
| ISSN: | 0166-4328 |
| DOI: | 10.1016/j.bbr.2016.12.038 |
| Popis: | BACKGROUND: Thalamic dysfunction has been implicated in overall chronic neurological dysfunction after traumatic brain injury (TBI), however little is known about the underlying histopathology. In experimental diffuse TBI (dTBI), we hypothesize that persisting histopathological changes in the ventral posteromedial (VPM) nucleus of the thalamus is indicative of progressive circuit reorganization. Since circuit reorganization in the VPM impacts the whisker sensory system, the histopathology could explain the development of hypersensitivity to whisker stimulation by 28 days post-injury; similar to light and sound hypersensitivity in human TBI survivors. METHODS: Adult, male Sprague-Dawley rats underwent craniotomy and midline fluid percussion injury (FPI) (moderate severity; 1.8–2.0 atm) or sham surgery. At 1d, 7d, and 28 days post-FPI (d FPI) separate experiments confirmed the cytoarchitecture (Giemsa stain) and evaluated neuropathology (silver stain), activated astrocytes (GFAP), neuron morphology (Golgi stain) and microglial morphology (Iba-1) in the VPM. RESULTS: Cytoarchitecture was unchanged throughout the time course, similar to previously published data; however, neuropathology and astrocyte activation were significantly increased at 7d and 28d and activated microglia were present at all time points. Neuron morphology was dynamic over the time course with decreased dendritic complexity (fewer branch points; decreased length of processes) at 7d FPI and return to sham values by 28d FPI. CONCLUSIONS: These data indicate that dTBI results in persisting thalamic histopathology out to a chronic time point. While these changes can be indicative of either adaptive (recovery) or maladaptive (neurological dysfunction) circuit reorganization, they also provide a potential mechanism by which maladaptive circuit reorganization could contribute to the development of chronic neurological dysfunction. Understanding the processes that mediate circuit reorganization is critical to the development of future therapies for TBI patients. |
| Databáze: | OpenAIRE |
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