Eberhart Zrenner

Slow and fast pathways in the human rod visual system: electrophysiology and psychophysics

Under most conditions, increasing the intensity of a flickering light makes the flicker more conspicuous. For a light flickering at 15 times per second, however, increasing the intensity can cause the flicker to disappear before reappearing again at higher intensities [Vision Res. 29, 1539 (1989)]. This flicker disappearance or null is also evident in human electrophysiological recordings at the same intensity levels. These results point to a duality within the rod visual pathway, in which flicker signals travel through a slow and a fast pathway and then recombine at a later stage. At 15 Hz the slow rod flicker signals are delayed by half a cycle relative to the fast signals. Thus, when the two signals are recombined, they destructively interfere and diminish the perception of flicker. The dual-pathway interpretation is supported by both electroretinographic and psychophysical evidence showing a phase difference of half a cycle between 15-Hz rod signals just below and just above the null region. These effects are apparent not only in the normal observer but also in an achromat observer who lacks functioning cone vision.

Linear Input Filters in Retinal Prosthetics

Introduction: Retinal prosthetics have made major progress over the past decade despite an incomplete understanding of how electrical stimulation activates the retina. A useful expansion of our understanding would be characterization of the linear input filter applied by the retinal circuit to extracellular[for full text, please go to the a.m. URL]

The Molecular Basis of Achromatopsia

Achromatopsia is a rare genetic heterogenic disorder with known loci on chromosome 2q11 (ACHM2) and chromosome 8q21 (ACHM3). These loci encode the genes for the channel-forming α- (CNGA3) and the modulatory (β-subunit (CNGB3) of the cone photoreceptor cGMP gated channel — the final component of the cone photoreceptor transduction cascade. Candidate gene screening of these genes in patients affect by Achromatopsia resulted in the identification of a large number of predominantly missense mutations in the CNGA3 gene and a discrete number of mostly nonsense mutations in the CNGB3 gene. Mutations in both genes result in Achromatopsia with clinically indistinguishable phenotypes.