December 2019
Volume 19, Issue 15
Open Access
OSA Fall Vision Meeting Abstract  |   December 2019
A Union of Light and Pain Pathways in Photophobia, in Sickness and in Health
Author Affiliations
  • Anna Matynia
    Associate Researcher Ophthalmologist, Director of Basic Research, Laboratory of Ocular Molecular and Cellular Biology and Genetics, Jules Stein Eye Institute, UCLA, DSERC Rm 3-128, 310-825-7519, matynia@jsei.ucla.edu
Journal of Vision December 2019, Vol.19, 12. doi:https://doi.org/10.1167/19.15.12
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      Anna Matynia; A Union of Light and Pain Pathways in Photophobia, in Sickness and in Health. Journal of Vision 2019;19(15):12. doi: https://doi.org/10.1167/19.15.12.

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

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Abstract

Background: Photoallodynia, a painful response to light, is a common symptom of migraine and corneal damage or inflammation. Melanopsin, best-known as the photopigment expressed in intrinsically photosensitive retinal ganglion cells (ipRGCs) at the heart of non-image forming vision, also plays an important role in light aversion, a surrogate for photoallodynia. These studies investigate the interaction between light and pain pathways using light aversion in mouse models of disease or injury.

Methods: We used mouse models of corneal injury and migraine to evaluate light aversion behavior. Genetic mouse strains, surgical lesions and pharmacological conditions were employed to dissect relative contributions of image based vision (rod and cone photoreceptors) and non-image based light perception (melanopsin-containing neurons), and investigate melanopsin expression in the trigeminal system. Von frey fibers were used to assess corneal sensitivity.

Results: Light aversion in pathophysiological states can be dissociated from optic nerve light transmission (encompassing rods, cones and ipRGCs) after optic nerve crush or transection, indicating the existence of non-ocular light detecting pathways. We have demonstrated the expression of melanopsin outside of the retina, in small and medium-sized trigeminal ganglion neurons (mTGs), and have shown that these cells are capable of light-regulated excitation. Loss of all melanopsin-expressing neurons (ipRGCs and mTGs) reduces both innate and corneal surface damage-induced light aversion but migraine-related light aversion persists through rod and cone pathways. Loss of mTGs also reduces corneal touch sensitivity, indicating a direct role for mTGs in the cornea.

Conclusions: The neural pathways contributing to light aversion are dependent on disease and its etiology. In healthy conditions, the retina and optic nerve are the predominant mediators of light aversion. By contrast, multiple pathways for light aversion are recruited in pathological states. The same trigeminal ganglion neurons that mediate pain responses to chemical and mechanical stimuli may also respond to light in order to “turn up the gain” for light-induced behaviors. These sensitized pathways may help limit exposure to potentially damaging light, or direct an animal to hide from predators during recovery from sickness or injury.

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