June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Acute corneal epithelial debridement in rats unmasks the corneal stromal nerve responses to ocular stimulation: Implications for abnormal sensations in recurrent corneal erosion and dry eye disease.
Author Affiliations & Notes
  • Harumitsu Hirata
    Ophthalmology, Weill Cornell Medical College, New York, New York, United States
  • Kamila Mizerska
    Ophthalmology, Weill Cornell Medical College, New York, New York, United States
  • Valentina Dallacasagrande
    Ophthalmology, Weill Cornell Medical College, New York, New York, United States
  • Victor H Guaiquil
    Department of Ophthalmology and Visual Sciences, University of Illinois-Chicag, Chicage, Illinois, United States
  • Mark Rosenblatt
    Department of Ophthalmology and Visual Sciences, University of Illinois-Chicag, Chicage, Illinois, United States
  • Footnotes
    Commercial Relationships   Harumitsu Hirata, None; Kamila Mizerska, None; Valentina Dallacasagrande, None; Victor Guaiquil, None; Mark Rosenblatt, None
  • Footnotes
    Support  NIH Grants EY023555, EY018594, and the Research to Prevent Blindness Grants to Department of Ophthalmology, Weill Cornell Medical College.
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 479. doi:
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      Harumitsu Hirata, Kamila Mizerska, Valentina Dallacasagrande, Victor H Guaiquil, Mark Rosenblatt; Acute corneal epithelial debridement in rats unmasks the corneal stromal nerve responses to ocular stimulation: Implications for abnormal sensations in recurrent corneal erosion and dry eye disease.. Invest. Ophthalmol. Vis. Sci. 2017;58(8):479.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : It is widely accepted that the mechanisms for transducing sensory information reside in the nerve terminals (NTs). Occasionally, however, studies have appeared demonstrating that similar mechanisms may exist in the axon to which these NTs are connected. We examined this issue using the cornea where NTs in the epithelial cell layers are easily accessible for debridement, leaving the underlying stromal (axonal) nerves (SNs) undisturbed.

Methods : In isoflurane-anesthetized rats, we recorded extracellularly from single trigeminal ganglion neurons innervating the cornea. Two types of corneal neurons, low threshold cold-sensitive plus dry sensitive (LT-CS+DS) and high threshold cold-sensitive plus dry sensitive (HT-CS+DS) neurons, were studied in response to a variety of ocular stimuli before and after the epithelial debridement. We previously hypothesized that these neurons play a critical role in tearing and ocular pain. Immunohistochemical techniques were also used to confirm the extent and the consistency of the debridement lesions.

Results : We found that the responses in both types of neurons to dryness, wetness, and menthol stimuli applied to the ocular surface were completely abolished by epithelial debridement, while a significant amount of the responses to the cold, heat and hyperosmolar stimuli (HOS) in LT-CS+DS neurons (but not HT-CS+DS neurons) still remained even after debriding the areas of the cornea that far exceeded the neurons’ receptive fields. Surprisingly, the responses to heat in ~ half of the neurons tested were augmented after the debridement. We were also able to evoke these residual responses and follow the trajectory of the SNs, which we subsequently confirmed histologically. The residual responses always disappeared when the the limbus, where the SNs originate, was cut.

Conclusions : In addition to the transduction mechanisms in the NTs giving rise to the responses to ocular dryness and menthol, this study provides strong evidence that the additional transduction mechanisms for the sensory modalities, such as cold, heat and HOS responses, originate in SNs. The functional significance of these residual and enhanced responses from SNs may be related to the abnormal sensations observed in a variety of ocular disease and symptoms.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

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