Targeted surface marker screening on neuronal structures in the human choroid.

While choroidal neuronal control is known to be essential for retinal and ocular health, its mechanisms are not understood. Especially, the local choroidal innervation mediated by intrinsic choroidal neurons (ICN) remains enigmatic. Neuronal functionality depends on the synaptic neurotransmitters and neuroregulatory peptides involved as well as from membrane components presented on the cell surface. Since the neuronal surface molecular expression patterns in the choroid are currently unknown, we sought to determine the presence of various cluster-of-differentiation (CD) antigens in choroidal neuronal structures with a particular focus on ICN. Human choroids were prepared for immunohistochemistry and the pan-neuronal marker PGP9.5 was combined with CD15, CD24, CD29, CD34, CD46, CD49b, CD49e, CD56, CD58, CD59, CD71, CD81, CD90, CD146, CD147, CD151, CD165, CD171, CD184, CD200, CD271 and fluorescence- and confocal laser scanning-microscopy was used for documentation. The following antigens were found to be co-localized in PGP.9.5+ nerve fibers and ICN perikarya: CD29, CD34, CD56, CD81, CD90, CD146, CD147, CD151, CD171, CD200 and CD271, while all other CD markers where not detectable. Whereas CD24- and CD59- immunoreactivity was clearly absent in ICN perikarya, some neural processes of the choroidal stroma displayed CD24 and CD59 immunopositivity. While a multitude of the aforementioned CD-markers were indeed detected in nervous structures of the choroid, the CD24+ and CD59+ nerve fibers most likely have extrinsic origin from cranial ganglia since ICN cell bodies were found to lack both markers. These findings illustrate how the detailed analysis of CD molecules described here opens novel avenues for future functional studies on choroidal innervation and its control.

The choroid-sclera interface: An ultrastructural study.

Emmetropization is an active and visually guided process that involves the retina, choroid and sclera, and results in compensatory changes in eye growth. This guided growth is the result of visual cues and possibly mechanical interactions being translated into growth signals via molecular events from the retina into the choroid and sclera, through the choroidal scleral transition zone. If mechanical interactions were a part of the choroid-sclera signaling transduction cascade, specific morphological arrangements should be detectable in this region at the ultrastructural level. The goal of this study was to investigate the ultrastructural features of the choroidal scleral transition zone by comparing avian, non-human primate and human eyes, with the goal to confirm whether specific mechanical structures are present. Choroidal and scleral tissue from chicken, marmoset, and human eyes were imaged using transmission electron microscopy to document the choroid-sclera transition zone. In chicken eyes, fibroblast lamellae bordered the scleral matrix and formed thin end elongated processes that were undercut by scleral collagen fibrils. These processes back-looped into the scleral matrix, and displayed small club-like membrane protrusions. Differences in these arrangements in mature vs young chickens were not detected. The club-like membrane protrusions identified in chickens were rare in marmoset eyes, which instead exhibited two types of collagen fibrils discriminated by size, and were absent in the human eyes investigated. In marmoset and human eyes, elastic components were detected in the transition zone that were absent in chickens. In summary, cellular/membrane specializations indicating a mechanical interaction at the choroid-sclera transition zone were not detected in chicken, non-human primate or human eyes. If mechanotransduction is necessary for scleral growth, matrix integrity or development, alternative structural arrangements might be required.