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Neurodegenerative diseases, like Alzheimer’s or Parkinson’s disease, lead to irreversible damage in the central nervous system in mammals, which might occasionally result in death. This because mammals are unable to repair or replace lost neurons in the central nervous system, and cannot repair damaged neuronal extensions, despite intense research efforts to stimulate these processes. However, up till now, research efforts mainly focus on the regeneration of the long extensions (axons). In contrast, contribution of the short neurites (dendrites) in the process of induction of regeneration is regularly neglected. Consequently, it is very interesting to investigate if, and how these dendrites contribute to the axonal regeneration process. The possible connection between these processes is studied in zebrafish, as they are, in contrast to mammals, capable of both replacement and repair in the damaged central nervous system. Furthermore, these interactions are regularly studied in the retina of the eye, as this is one of the most accessible parts of the central nervous system. In this thesis, it is demonstrated that following optic nerve injury in the zebrafish, in which the axons are damaged, axons will regrow, and concurrently, dendrites will start to shrink. Therefore, a functional relationship between these two processes is suggestive, where this retraction of the dendrites could be essential to obtain enough energy for successful axonal regeneration. This idea is reinforced, by our results from experiments where the effects of inhibition of an important factor in the energy metabolism, namely mTOR, were studied. mTOR inhibition impedes axonal regeneration, and possibly hampers dendritic retraction after optic nerve injury in zebrafish. Hence, mTOR could be proposed as a possible link, declaring the observed connection. Additionally, also a short increase in autophagy is observed following optic nerve injury. Autophagy, as a recycling mechanism in cells, could likewise provide the energy needed for axonal regeneration, and could therefore be presented as an alternative explanation for the observed connection. Although more experiments are needed, as a conclusion for this thesis we suggest that a temporal dendritic retraction could be needed to enable regrowth of axons following optic nerve injury in zebrafish. Moreover, we suggest an important function for mTOR as energetic link between these two processes, where autophagy could play an ancillary role.