Edge sensitive mechanisms in humans with abnormal visual experience.

Detection of broadband, aperiodic stimuli (edges) was investigated in normal observers, and in observers with abnormal visual experience which resulted in amblyopia. The spatial properties of the mechanisms used to detect an edge were investigated by a method of subthreshold addition. The method involved the determination of the threshold contrast for detecting an edge in the presence of a subthreshold line at various distances from the edge. In normal eyes, the one dimensional sensitivity profile of the edge detecting mechanism was: (1) approximately antisymmetric, (2) very localized, with sensitivity changes restricted to +/- 6'--8' on either side of the edge, and (3) phase dependent, showing an abrupt change in sign between +/- 1.5'. The sensitivity profiles of the amblyopic eyes were also approximately antisymmetric and showed the same steep rate of change from plus to minus as the fellow (nonamblyopic) eyes. However, in every case, the spatial extent of the profile was much broader than that of the nonamblyopic eyes. In normal eyes, the narrowest edge sensitivity profile was associated with the fovea; however, in two amblyopes with eccentric fixation, the narrowest edge sensitivity profile coincided with the locus of eccentric fixation. Moreover, the grating sensitivity function of the edge detecting mechanism of the amblyopic eye was similar to that of the non-amblyopic eye, but was shifted toward lower spatial frequencies. Control experiments show that these results are not accounted for on the basis of optics, eccentric fixation, or abnormal eye movements. The findings are discussed in terms of current models for the detection of aperiodic stimuli, and in the context of animal models of amblyopia.

Reticuloendothelial and mesangial function in murine immune complex glomerulonephritis.

The function of the mesangial and reticuloendothelial system was evaluated in normal mice and in mice with nephritis induced by lymphocytic choriomeningitis (LCM) virus infection. Heat-aggregated human immunoglobulin (AlgG) and colloidal carbon served as traceable materials which could be detected in animals' blood and tissues. LCM virus-infected proteinuric (LCM-P) mice, as compared to normal mice or LCM-infected nonproteinuric (LCM) mice, had greater accumulation of AIgG in their glomeruli at all times of examination following i.p. injection of AIgG. The removal rate of AIgG from the kidney, however, was the same in normal and LCM-P mice, indicating an unimpaired mesangial clearing system. This suggested that other mechanisms were responsible for the increased glomerular accumulation of AIgG in LCM-P mice. Reticuloendothelial function was examined directly by i.v. injection of AIgG or colloidal carbon. The data demonstrate that in this model of immune complex glomerulonephritis, colloidal material tested was removed from the blood at a slower rate than it was in normal mice. Deficient clearance of endogenous blood-borne immune complex-like material may be one of the factors playing a role in the accumulation of immune complex-like material in the glomeruli of these nephritic animals.