Function and Structure of Damaged and Regenerating Corneal Cold Sensitive Nerves

Corneal sensory nerves help protect the ocular surface from damage. Although these nerve endings are able to regenerate from injury, their structure and function can be compromised leading to pain and propagating ocular surface damage. Corneal cold sensitive nerves are the major subtype regulating ocular surface homeostasis. By using extracellular electrophysiology of the trigeminal ganglion combined with immunohistochemistry, this work seeks to show the consequences of corneal nerve damage and regeneration on both the structure and function of corneal cold sensitive nerves. First, it is demonstrated that Benzalkonium chloride (BAK), a common ocular drop preservative, damages the nerve endings of corneal cold sensitive nerves. Subsequently the consequences of corneal regeneration from BAK or ocular debridement injuries are demonstrated, highlighting that different injury models may lead to prolonged and differential effects on corneal nerve properties after regeneration. The findings of this dissertation work help to elucidate the sensory disturbances experienced by people who experience ocular surface damage due to iatrogenic or traumatic causes.