a1 Center for Ultrastructural Research, University of Agriculture, Vienna
a2 Department of General and Comparative Physiology, Medical School, University of Vienna
a3 University Eye Clinic, Medical School, University of Vienna
The quality of the foveal cone mosaic in human and primate retinas is a basic parameter of spatial vision function. The present study uses digital-texture analysis procedures to analyze the crystalline order of inner segment sections containing the rod-free portions of foveal cone mosaics. Definition of the cone cross-sectional centers made possible by adequate preprocessing allows precise mapping of lattice vertices and differentiation of hexagonal positions by procedures for direct neighbor recongnition.
In a further step, the existence of subunits within the hexagonal areas is revealed by the determination of axial orientation. The lattice of the subunits is characterized by similar orientation and high positional correlation of its hexagonal units.
The axial orientation of the areas differs from that of neighboring subunits by angular shifts of 10–15 deg and linear series of nonhexagonal irregularities demarcate the borders. Although larger patches with continuous hexagonal order occur in the surrounding rod-free regions, elevated degrees of disorder (30%) are found within the foveolar center (ca. 300 cones). Analysis of a mosaic showing labeled B cones (Szél et al., 1988) demonstrates that lattice disorder is in part associated with the blue cone subpopulation. The foveal mosaic from a glaucomatuous eye reveals severe lattice degradation throughout the rod-free zone, presumably due to extensive receptor loss.
The low-frequency superstructure results in local sets of sampling grids (5'–8') with differing orientational bias. Besides a horizontal/vertical difference of mosaic compression (ca. 1:1.15), the present analysis gives no hints for the existence of systematic meridional anisotropies at the receptor mosaic level. The study reveals a discontinuous organization of the foveal mosaic and points to possible sources for the induction and location of lattice disorder.
(Received February 01 1988)
(Accepted June 27 1990)
Reprint requests to: Peter K. Ahnelt, Department of General and Comparative Physiology, Medical School, University of Vienna, Schwarzspanierstr. 17, A-1090 Vienna, Austria.