*3.2. Repetitive mTBI Did Not Cause Neurodegeneration, Changes in the Responses of Glial Cells, and Synaptic Reorganization in the Lateral Geniculate Nucleus and the Superior Colliculus in Wild-Type and TDP-43G348C Mice at 6 Months Following the Last Head Impact*

To the best of our knowledge, we are the first group to explore possible chronic damage, glial activity, and synaptic organization in the LGN and the SC following repetitive mTBI in mice of both genotypes.

The LGN, situated in the thalamus, was reported to receive external visual information mostly by the axons of the retinal ganglion cells, conducting them to the visual cortex [71]. The SC has a laminar structure, and its three superficial layers are primarily visual sensory in nature [72]. In mice, the SC also receives the projections, but from at least 70% [73] and possibly even approximately 88% of the retinal ganglion cells [74].

In the current study, no signs of neurodegeneration in the LGN and only a few scattered Fluoro-Jade C-positive signals in the superficial SC were detected in the injured mice of both genotypes. Additionally, when using cresyl-violet, no differences were revealed in the neuronal density between the injured wild-type and TDP-43 transgenic mice compared with their related sham or between traumatized wild-type and TDP-43G348C mice. Considering the abovementioned results, we suggest that repetitive mTBI did not induce chronic damage of the target nuclei and that the investigated genotype did not influence it. Furthermore, reactive microgliosis or astrocytosis were not detected. Previously, microglial infiltration and activation in the SC were found 7 days after the last head trauma [50]. In the same research, the injury of the LGN was mentioned [50]. Both results were obtained using a method of repeated head traumas different from ours.

The central nervous system has the capacity of neuroplasticity and recovery following different insults that include various processes, ranging from molecular, cellular, and synaptic to global [75]. Some of these processes are associated with changes in the expression of different specific proteins, synaptogenesis markers, and synapse remodeling, such as SYP [76–79]. In our study, no differences in the SYP immunostaining intensities between the experimental groups were detected, suggesting that repetitive mTBI or the genotype did not induce synaptic perturbations in the LGN or the SC at 6 months following repetitive mTBI. To our knowledge, synaptogenesis markers have not been previously studied in the LGN and the SC following repeated head traumas.
