Sympathetic innervation of the developing aqueous humor drainage structures.

Haelynn Gim

Document Type

Article

Publication Date

Summer 2017

JAX Location

In: Student Reports, Summer 2017, Jackson Laboratory

Abstract

This study mapped the sympathetic innervation of the developing aqueous humor (AQH) drainage structures in mice at specific postnatal ages from Pl.5 to no. An increase in resistance to AQH outflow leads to an elevated intraocular pressure (lOP). This ocular hypertension is a key risk factor for glaucoma, a neurodegenerative disease which leads to irreversible loss of vision. Research has suggested that neuronal regulation may be a plausible mechanism controlling lOP and the outflow of AQH through the drainage structures, which include Schlemm's canal and the trabecular meshwork in the primary outflow pathway. Research in the John lab has detected neuronal innervation of both sympathetic and parasympathetic nature in the adult mouse AQH drainage structures , particularly near the inner wall of SC, which is the last barrier to outflow . To expand upon this work, this project examined the development of sympathetic innervation as SC forms, employing immunohistochemistry, a fluorescent transgenic strain, an anterior segment whole-mounting technique, and confocal imaging. Sympathetic innervation of SC did not appear to begin until P8, much after the initiation of SC development, and increased with age. This later development of innervation may possibly suggest that neuronal regulation of AQH drainage structures does not begin until these structures become functional, although the exact age at which AQH outflow through this pathway begins is unknown. In contrast, the neighboring vasculature appeared to have robust neuronal presence even at PI.5. These blood vessels are likely to playa role in lOP; thus their early and continued innervation may be of significance. Understanding the mechanisms for AQH outflow and lOP regulation is an important early step in the development of human glaucoma treatment options that directly target neurons to lower lOP.

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