## 3 Discussion  
Mitochondrial dysfunction is a cause of lower metabolic activity in glaucoma patients, which in turn represents stress conditions for retinal cells, especially retinal ganglion cells (RGCs), resulting in cell death. These processes are similar in glaucoma patients and animal models [23]. The animal model used in this study induced chronic IOP elevation in Sprague Dawley rats by occluding three of four episcleral veins (EVO) of the OS to mimic glaucomalike conditions [24]. EVO resulted in a significantly increased IOP, which remained stable until the end of the study and had similar levels as in previous studies of our group [25,26]. Additionally, the significant loss of RGCs and the magnitude of RNFLT thinning in the IgG OS group were within the expected range [25, 26, 27]. Considering the regional RGC density (Figure 2), it was noticeable that the protective effect of anti-DNM1L Ab mostly occurred in the central and mid-peripheral regions. As the pressure sensitivity of RGCs increases towards the periphery, RGC survival in our study could be caused by RGCs, which have not fully activated the apoptosis signaling pathways yet [28, 29, 30]. Additionally, the viable RGCs might be capable of regeneration instead of going into apoptosis [31,32]. Regarding retinal functionality, chronic IOP elevation in ERG patterns showed a noticeable decrease in B-wave amplitude in a similar range compared to another study [27]. However, it points out that not only inner but also outer retinal layers were affected by chronic IOP elevation. This might be caused by photoreceptor cells affected by IOP, as \begin{table}
\begin{tabular}{c c c} \hline \hline \multicolumn{3}{c}{**MS Identified Proteins, Which Are Located in Mitochondria**}. \\ \hline \hline
**Protein Name** & **Protein Name** & **Abbreviated** & **Regulation in the DNMIL OS Group** \\ \hline Glutamate dehydrogenase 1 & CLUDI & Down \\ ADP/ATP translocae 2 & SLC25A5, ANT2 & Down \\ mitochondrial stress-70 protein, & HSPA9 & Up \\ mitochondrial & & \\ \hline \hline
**MS Identified Proteins** & **Associated with the Cytoskeleton**. \\ \hline \hline
**Protein name** & **Protein name** & **Repetition in the DNMIL OS Group** \\ \hline Neuronal growth factor 1 & NEGR1 & Down \\ Coatosin-like protein 1 & COTL1 & Down \\ Tubulin polymerization promoting protein & TPPP & Up \\ Microtubule-associated protein 1A & MAP1A & Up \\ \hline \hline
**MS Identified Proteins** & **Associated with vesicle Traffic**. \\ \hline \hline
**Protein name** & **Protein name** & **Repetition in the DNMIL OS Group** \\ \hline Clathrin coat assembly protein AP180 & SNAP91 & Up \\ \hline Vesicle fusing ATPase & NSF & Up \\ \hline V-type proton ATPase subunit & ATP6V1E1 & Up \\ \hline ADP-ribosylation factor 1 & ARF1 & Up \\ \hline Synaptlogamin-1 & SYT 1 & Up \\ \hline Synaptic vesicle glycoprotein 2A & SV2A & Up \\ \hline alpha-Synuclein & SCNA & Up \\ \hline beta-Synuclein & SCNB & Up \\ \hline \hline \end{tabular}
\end{table} 
Table 1: MS identified proteins, categorized by subcellular location or association. shown by [PERSON] et al. (2000) [33]. A lower PhNR amplitude was expected since it mainly originated from the RGCs, which were remarkably decreased due to the IOP elevation. Injection of the anti-DNM1L Abs mitigated the reduction in PhNR amplitude compared to the control IgG, probably due to the neuroprotection of RGCs in the antibody-treated eyes. Nevertheless, it should be noted that the preservation of structure does not necessarily imply a positive effect on functionality. Indeed, ERG cannot determine from which RGC the electrophysiological response precisely originated. Nevertheless, it has previously been shown that targeting mitochondria, which enhances energy metabolism in RGCs, can positively affect retinal functionality, especially the PhNR [34, 35]. In summary, the present study demonstrated that anti-DNM1L Ab injection induced positive neuroprotective effects at both physical and physiological levels.