Corneal nerve ending

Corneal nerve endings are the terminal sensory fibers of the ophthalmic branch of the trigeminal nerve, constituting the most densely innervated tissue in the human body (StatPearls, 2023). These nerves, primarily A-delta and C fibers, form the subbasal nerve plexus and are vital for maintaining the physiological integrity of the ocular surface through the release of trophic neuromodulators like substance P and calcitonin gene-related peptide (PubMed, PMID: 28553924). They serve as the afferent pathway for the blink reflex and tear production, providing essential protective mechanisms against environmental damage (NIH, 2021). Pathological degradation of these nerve endings, known as neurotrophic keratitis, results in a loss of corneal sensation, impaired epithelial healing, and a high risk of corneal ulceration (FDA, 2018). Pharmacological interventions such as Cenegermin (recombinant human nerve growth factor) target these endings by binding to TrkA and p75NTR receptors to promote nerve survival and regeneration (PubChem, CID: 134694445). Additionally, these nerves are the site of action for local anesthetics, which block voltage-gated sodium channels to provide analgesia, though their chronic use is limited by the risk of secondary corneal damage.

Other names

Corneal sensory nerveCorneal subbasal nerve plexusTrigeminal corneal fiberCorneal nociceptor

Stimulation of Nerve Growth Factor receptors (TrkA and p75NTR) to promote nerve survival and regeneration; inhibition of voltage-gated sodium channels to block nociceptive signal conduction.