Inflammation and neuroplasticity in the cornea

Abstract

Neuroplasticity is related to the addition of additional axon collaterals and dendrites between a nerve cell and one it has previously shared a connection in order to strengthen, re-establish or forge brand new connections with pre-existing neurons. The role of neuroplasticity following a wound to an epithelium such as the cornea is of great importance to vision science, as it may help shape future medical approaches to common eye injuries in such a way that chronic eye pain and even blindness can be avoided. The present study suggests that Mus musculus is a viable model for the study of changes in nerve morphology and density that are correlated with neuroplasticity. Furthermore, the work presented here suggests a possible correlation between peak immune cell infiltration of the cornea and the initiation of changes in nerve density and organisation related to neuroplasticity. After significant (P<0.05) decrease in the density of both major nerves and neuronal processes following chemical cauterization with silver nitrate, the density of both major nerves and nerve processes increased a significant (P>0.05) amount when mice were allowed to recover for up to 48 hours after treatment. Interestingly, nerve processes increased by 31.4% in only 48 hours. These results suggest that neuroplasticity is observed in the cornea following an injury. This study also shows that macrophage and neutrophil infiltration of the stroma peaks at around the same time that the cornea begins to regain some nerve density, suggesting that there may be a link between these two wound healing processes in the corneas of mice and potentially other mammals, including humans.