Structural and ultrastructural changes to the sclera in a mammalian model of high myopia.

PURPOSE: The development of high myopia is associated with scleral thinning and changes in the diameter of scleral collagen fibrils in humans. In the present study, the association between these scleral changes and the losses in scleral tissue that have previously been reported in animal models were investigated to determine the relationship between changes in collagen fibril architecture and thinning of the sclera in high myopia. METHODS: Myopia was induced in young tree shrews by monocular deprivation of pattern vision for short-term (12 days) or long-term (3-20 months) periods. Scleral tissue from normal animals over a wide age range (birth to 21 months) was also collected to provide data on the normal development of the sclera. Light and electron microscopy were used to measure scleral thickness and to determine the frequency distribution of collagen fibril diameters in the sclera. Tissue loss was monitored through measures of scleral dry weight. RESULTS: Significant scleral thinning and tissue loss, particularly at the posterior pole of the eye, were associated with ocular enlargement and myopia development after both short- and long-term treatments. However, collagen fibril diameter distribution was not significantly altered after short-term myopia treatment, whereas, from 3 months of monocular deprivation onward, significant reductions in the median collagen fibril diameter were noted, particularly at the posterior pole. CONCLUSIONS: The results of this study demonstrated that loss of scleral tissue and subsequent scleral thinning occurred rapidly during development of axial myopia. However, this initial tissue loss progressed in a way that did not result in significant alterations to the collagen fibril diameter distribution. In the longer term, there was an increased number of small diameter collagen fibrils in the sclera of highly myopic eyes, which is consistent with findings in humans and is likely to contribute to the weakened biomechanical properties of the sclera that have previously been reported.

The effects of blockade of retinal cell action potentials on ocular growth, emmetropization and form deprivation myopia in young chicks.

To investigate the influence of brain mediated functions on control of ocular growth, young chicks were treated monocularly with intravitreally injected tetrodotoxin (TTX) to block retinal ganglion cell action potentials. TTX injections (0.7 micrograms in 7 microliters) were given on day 6 after hatching in both binocularly open and monocularly deprived chicks. Injections were repeated every 48 hr for a period of 8 days (TTX-open; TTX-MD). Control groups of animals received intravitreally injected phosphate buffered saline (PBS-open; PBS-MD) to one eye on the same schedule. There was a minimum of eight animals in each group. Recovery from form-deprivation myopia during blockade of retinal cell action potentials was also investigated. Results demonstrate that blockade of retinal cell action potentials by TTX produces reduced growth of the anterior segment of the eye and crystalline lens in both binocularly open and MD chicks. Blockade of retinal cell action potentials does not prevent form-deprivation induced vitreous chamber elongation and myopia. Form deprived myopic eyes were found to emmetropize despite blockade of retinal ganglion cell action potentials giving further evidence for local ocular control of emmetropization. Blockade of retinal ganglion cell action potentials did not prevent changes in choroidal thickness in eyes developing axial myopia or eyes recovering from induced myopia.

Eusynstyelamide, a highly modified dimer peptide from the ascidian Eusynstyela misakiensis.

Eusynstyelamide, a novel peptide derivative from the ascidian Eusynstyela misakiensis, was isolated and characterized by spectroscopic methods.