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Biomedical subjects

Steven F Stasheff

Publications and source records attributed to Steven F Stasheff.

3 recordsLinked to original sources

Visual dysfunction in retinal and optic nerve disease.

Visual perceptions seen with retinal and optic nerve disease may overlap with those resulting from retrochiasmal disorders. A few disorders typically present with distinctive perceptions, but the majority have less specific symptoms. Features include whether or not the visual phenomena are negative or positive, monocular or binocular, and the location and form of any deficits. Among negative phenomena, transient visual loss usually is the result of ischemic disease, but particular precipitants may suggest demyelination or photoreceptor degeneration. The pattern and location of visual field defects may help localize disorders to the level of the macula, papillomacular or other inner retina nerve fiber bundles, optic nerve, or chiasm. Altered brightness perception may point to optic nerve or photoreceptor disease. Decreased acuity is among the most common and least specific symptoms, but association with other symptoms may help to narrow the differential diagnosis. Dyschromatopsia points to either a photoreceptor or optic nerve pathologic condition (Table 7). Among positive phenomena, hallucinations resulting from anterior visual system disorders typically are unformed, although deafferentation of retrochiasmal pathways may produce formed hallucinations. The common "floaters" frequently are benign, but occasionally herald more concerning disorders. Various types of photopsias commonly occur with vitreal disorders or photoreceptor disorders. Macular disease typically leads to distortions of the central visual field, and other particular disorders lead to a host of characteristic distortions of color, form, or brightness. Careful attention to the ophthalmologic examination, visual fields, and subtle variance in symptomatology also help to distinguish among various disorders.

Color Vision Defects↗

Pattern of synaptic excitation and inhibition upon direction-selective retinal ganglion cells.

The distributions of excitatory and inhibitory synapses upon the dendritic arbor of a direction-selective retinal ganglion cell were compared by triple-labeling techniques. The dendrites were visualized by confocal microscopy after injection of Lucifer yellow. Excitatory inputs from bipolar cells were located by using antibodies against kinesin II, a component of synaptic ribbons. Inhibitory inputs were identified by antibodies against gamma-aminobutyric acid-A receptors. The combined images were examined by visual inspection and by formal, automated analyses, in a search for anisotropies that might contribute to a directional preference of the ganglion cell. Within the limits of our analysis, none was found. If an anatomic specialization underlies direction selectivity, it appears to lie in the geometry and spatial positioning of the neurons afferent to the ganglion cell and/or the microcircuitry among its afferent synapses.

Animals↗

Functional inhibition in direction-selective retinal ganglion cells: spatiotemporal extent and intralaminar interactions.

We recorded from ON-OFF direction-selective ganglion cells (DS cells) in the rabbit retina to investigate in detail the inhibition that contributes to direction selectivity in these cells. Using paired stimuli moving sequentially across the cells' receptive fields in the preferred direction, we directly confirmed the prediction of that a wave of inhibition accompanies any moving excitatory stimulus on its null side, at a fixed spatial offset. Varying the interstimulus distance, stimulus size, luminance, and speed yielded a spatiotemporal map of the strength of inhibition within this region. This "null" inhibition was maximal at an intermediate distance behind a moving stimulus: 1/2 to 11/2 times the width of the receptive field. The strength of inhibition depended more on the distance behind the stimulus than on stimulus speed, and the inhibition often lasted 1-2 s. These spatial and temporal parameters appear to account for the known spatial frequency and velocity tuning of ON-OFF DS cells to drifting contrast gratings. Stimuli that elicit distinct ON and OFF responses to leading and trailing edges revealed that an excitatory response of either polarity could inhibit a subsequent response of either polarity. For example, an OFF response inhibited either an ON or OFF response of a subsequent stimulus. This inhibition apparently is conferred by a neural element or network spanning the ON and OFF sublayers of the inner plexiform layer, such as a multistratified amacrine cell. Trials using a stationary flashing spot as a probe demonstrated that the total amount of inhibition conferred on the DS cell was equivalent for stimuli moving in either the null or preferred direction. Apparently the cell does not act as a classic "integrate and fire" neuron, summing all inputs at the soma. Rather, computation of stimulus direction likely involves interactions between excitatory and inhibitory inputs in local regions of the dendrites.

Action Potentials↗