engleski

Neuronal damage and recovery in the thalamus following traumatic brain injury in the rat

Traumatic brain injury (TBI) is the leading cause of death and disability in population under the age of 45 years worldwide and thus represents a serious public health problem. TBI affects many brain regions, but the most studied are cortex and hippocampus, even though it has been documented that neurodegeneration and apoptosis are also present in other parts of the brain. Moreover, the process of reorganization in those, rarely examined brain regions has not been fully clarified. The purpose of this study was to determine the changes in several markers of neuronal damage and recovery in the thalamus following experimental TBI in the rat. Moderate TBI was induced using the lateral fluid percussion (LFP) brain injury model. Briefly, craniotomy was performed over the left parietal cortex and a plastic Luer Lock fitting was attached to the craniotomy site. This assembly was used to connect the animal to the LFP device and after that the brain injury was induced. Sham-operated animals were used as the control group. Rats were sacrificed 24 h or 72 h after the TBI induction or sham procedure. Animals were perfused and postfixed with 4% paraformaldehyde, their brains were paraffin-embedded and prepared for histological analyses. Brain sections were analyzed by Fluoro Jade B staining or by immunohistochemistry. Number of neurons was determined by NeuN staining. Neuroplastic responses were determined by immunofluorescent labeling of synaptophysin and growth-associated protein 43 (GAP-43). Neurodegenerative changes, marked by the increase in Fluoro Jade B staining, and significant neuronal loss were apparent in the thalamus following LFP injury. Intensity of GAP-43 staining was not significantly changed in the examined brain region after TBI. Increased signal intensity of synaptophysin was detected in the thalami of rats sacrificed 72 h after brain trauma. Results of this study suggest significant early neuronal thalamic damage following LFP injury in the rat. Furthermore, as soon as 3 days after brain trauma accumulation of synaptophysin within the thalamus reflects possible injury- induced recovery processes.

Neuronal damage; neuronal reorganization; traumatic brain injury; rat

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