Corneal innervation and sensation

Recent abstract.... These are the sorts of papers we've waited so many years to see.

May there be more every month. 

Yale J Biol Med. 2018 Mar 28;91(1):13-21. eCollection 2018 Mar.

Corneal Innervation and Sensation: The Eye and Beyond.

Yang AY1, Chow J1, Liu J1.
Department of Ophthalmology and Visual Science, Yale School of Medicine, New Haven, CT.

Abstract

The cornea is one of the most densely innervated and sensitive tissues in the body. In addition to their important sensory functions, corneal nerves induce reflex tear production, blinking, and the release of trophic factors - all of which combined help to maintain the structural and functional integrity of the surface of the eye. Consequently, damage to corneal nerves as a result of disease, surgery, or trauma can lead to diminished corneal sensitivity, epithelial defects, and possible blindness. In this review, we describe commonly used tools that have provided considerable new information on corneal architecture and sensation in healthy and diseased corneas, with special emphasis on changes seen in herpes zoster ophthalmicus, corneal and other therapeutic ocular procedures, antiglaucoma medical therapy, aging, and diabetes. With its potential applications ranging from managing ocular-specific to systemic diseases, the study of corneal innervation has implications for future therapies extending beyond just the eye itself.

Study about Acute Corneal Epithelial Debridement

ABSTRACT: Acute corneal epithelial debridement unmasks the corneal stromal nerve responses to ocular stimulation in rats: Implications for abnormal sensations of the eye.

J Neurophysiol. 2017 Mar 1:jn.00925.2016. doi: 10.1152/jn.00925.2016. [Epub ahead of print]
Hirata H1, Mizerska KK2, Dallacasagrande VA2, Guaiquil VH3, Rosenblatt MI3.

Abstract

It is widely accepted that the mechanisms for transducing sensory information reside in the nerve terminals. Occasionally, however, studies have appeared demonstrating that similar mechanisms may exist in the axon to which these terminals are connected. We examined this issue using the cornea where nerve terminals in the epithelial cell layers are easily accessible for debridement, leaving the underlying stromal (axonal) nerves undisturbed. In isoflurane-anesthetized rats, we recorded extracellularly from single trigeminal ganglion neurons innervating the cornea that are excited by ocular dryness and cooling: low threshold (<2 and="" cooling="" high="" oc="" threshold="">2 oC) cold-sensitive plus dry sensitive (LT-CS+DS and HT-CS+DS) neurons, playing possible roles in tearing and ocular pain. We found that the responses in both types of neurons to dryness, wetness, and menthol stimuli were effectively abolished by the debridement, indicating that their transduction mechanisms lie in the nerve terminals. However, some responses to the cold, heat and hyperosmolar stimuli in LT-CS+DS neurons still remained. Surprisingly, the responses to heat in ~ half of the neurons were augmented after the debridement. We were also able to evoke these residual responses and follow the trajectory of the stromal nerves, which we subsequently confirmed histologically. The residual responses always disappeared when the stromal nerves were cut at the limbus, suggesting that the additional transduction mechanisms for these sensory modalities originated mostly likely in stromal nerves. The functional significance of these residual and enhanced responses from stromal nerves may be related to the abnormal sensations observed in ocular disease.

Copyright © 2016, Journal of Neurophysiology.