engleski

Synaptic changes without signs of neurodegeneration in the rostral cerebrum after traumatic brain injury in the rat

Traumatic brain injury (TBI) results from the primary damage of the brain tissue, followed by secondary events which can develop within days and months after the impact and usually contribute to further impairment. Most of the studies so far were focused on the TBI consequences at and near the injury site, even though there are many indications that damage could be widespread throughout the brain. Processes of synaptic damage, reorganization and repair following TBI could be very important for post-injury recovery, but are still very poorly investigated, especially in the brain regions located further away from the impact site. The purpose of this study was to investigate possible presence of neuronal damage and appearance of synaptic changes in different regions of the rostral cerebrum within a week after experimentally induced TBI in the rat. Adult male Wistar rats were subjected to TBI of moderate severity using lateral fluid percussion injury (LFPI), induced over the left parietal cortex. Sham-operated rats were used as the control group. Animals were sacrificed 1, 3 or 7 days after procedure and their brains were prepared for histological analyses. Fluoro-Jade B staining was used to detect neurodegenerative changes and immunohistological labeling of synaptophysin (SYP), growth associated protein 43 (GAP-43) and postsynaptic density protein 95 (PSD-95) for determination of neuroplastic responses. Even though neurodegenerative changes were not detected, we observed synaptic changes in some regions of the rostral cerebrum, which varied at different time points and with a different synaptic marker. Our study suggests that TBI causes synaptic changes in regions distant from the impact site, even when there is no obvious neural damage, in the first week following LFPI in the rat. This work has been supported by the University of Rijeka under the project uniri-biomed-18-204 to Ž.G.

traumatic brain injury, rostral cerebrum, plasticity, neurodegeneration, rat

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