Cells projecting into the commissure of the cat's superior colliculus were identified during extracellular recording by antidromic activation. Electrical stimulation of the ipsilateral optic tract evoked action potentials in the majority of commissural neurons. Response latencies of 1.4 ± 0.5 ms (mean ± S.D.) in a few cells indicated that some commissural neurons receive direct input from the axons of retinal Y–cells. Most commissural cells responded 5.9 ± 1.9 ms (mean ± S.D.) following optic tract shock, implying that the responsible pathway was composed of more slowly conducting axons or did not proceed directly to the colliculus. Results of previous studies of retinal inputs to cells in the deep tectal layers suggest that the later responses were mediated by an indirect Y pathway through the visual cortex.

The phosphorylation of photoexcited rhodopsin (Rho*) is thought to inactivate this receptor by inhibiting its interaction with the GTP-binding protein transducin (Gt). Here we report that the time course of phosphorylation-dephosphorylation after bright illumination of intact rod outer and inner segments (ROS-RIS) incubated in 33Pi can be altered if the ROS-RIS are first exposed to levels of dim illumination that cause light adaptation in these ROS-RIS. The dephosphorylation of >107 phosphorylated rhodopsin molecules/ROS following a bright flash can be blocked by prior dim continuous illumination (generating 103 Rho*/ROS/s) that cumulatively bleaches ≍ 105 rhodopsin molecules/ROS. The phenomenon has not been previously noted because these low levels of light are emitted as a result of Cerenkov radiation from the 32P isotope that is usually employed to monitor rhodopsin phosphorylation. The inhibition of rhodopsin dephosphorylation by dim conditioning illumination is observed in intact ROS-RIS but is lost when ROS-RIS are electropermeabilized or fragmented.

Visual-evoked potentials (VEPs) were recorded from the surface of the optic tectum of the freshwater turtle, Pseudemys scripta elegans, in response to phase reversal of square-wave gratings of different spatial frequency and contrast. The refractive state of a group of 12 turtles in air was assessed from VEPs by placing trial lenses in front of the eye. The group mean refraction did not differ significantly from emmetropia, as compared to 4.8 diopters of hyperopia when refracted retinoscopically. The difference was explained by the retinoscopic reflex originating from the interface between vitreous humor and retina. Peak VEP amplitude was approximately linear with log grating contrast; extrapolation to zero VEP amplitude yielded contrast thresholds as low as 1%. High spatial-frequency cutoffs ranged from 4.4–9.9 cycle/deg in different animals, the highest values corresponding to the intercone spacing in the area centralis and to behavioral measures of acuity in a related species.

Primate retinal bipolar cells synapsing with two adjacent cones (2C bipolars) are further described. Their synaptic contacts are either as the central (invaginating) component of the cone triads or as basal (flat) contacts on the membrane of the cone pedicle base. Correspondingly, their axons end either in the b (inner) half or in the a (outer) half of the inner plexiform layer. The shape and size of the axon terminals of 2C bipolars are indistinguishable from those of adjacent midget bipolars. Therefore 2C bipolars, like midget bipolars, probably synapse with midget ganglion cells. Two C bipolars have not been identified as connected to foveal cones. But they are not restricted to the retinal periphery, as has previously been supposed, since they occur, mixed with midget (single cone) bipolars, throughout all parts of the retina from about 2.5 mm to atleast 10.0 mm from the fovea. It is likely that 2C bipolars are a variant of the midget bipolars; and that they contact some members of the same population of cones, instead of the midgets. This paper briefly reviews, and raises some new, problems concerning our current understanding of the synaptic connectivity patterns of the midget, 2C, and diffuse cone bipolar cells.

Measurements were made of the ocular dimensions from living and frozen eyes of one species of freshwater turtle, Pseudemys scripta elegans, and of three species of marine turtles, Chelonia mydas, Dermochelys cariacea, and Eretmochelys imbricata. Estimates of refractive error by retinoscopy were also obtained with eyes in air and under water. The results suggest that unaccommodated eyes of all four species are approximately emmetropic in air but strongly hyperopic in water. Schematic eyes were calculated for each species in both air and water.

The major neurons and neural circuits that are involved in the transmission of color signals through the human retina to produce the color and spatially opponent P cell or midget ganglion cell responses are described. The older findings of single cone to midget bipolar connectivity is reviewed, and the single midget bipolar cell to midget ganglion cell connectivity as revealed by a recent serial section electron microscope study is described in detail. Our present knowledge concerning the discrimination of the blue-cone subtype from the other longer wavelength cones in the human at the outer plexiform layer is summarized, and our most recent findings concerning horizontal cell connectivity to the different spectral types of cones are discussed. Finally, a hypothetical pathway is proposed for color-opponent surrounds of midget ganglion cells using both horizontal cells at the outer plexiform layer and amacrine cell pathways at the inner plexiform layer.

Saccadic reaction times (SRTs) of three human subjects were analyzed. The gap paradigm was used (i.e. fixation point offset precedes target onset) to obtain high proportions of express saccades (i.e. saccades of extremely short reaction times) in the SRT distributions. In one set of experiments, the luminance of the (red) saccade target was varied from brighter to darker than the (green) background including an isoluminance condition. Express saccades were obtained in response to pure color contrast stimuli with about the same frequency and reaction time as to stimuli with both color and luminance contrast. In a second experiment, the luminance contrast of a white target on a white background was lowered below 10%. Again the number of express saccades was not reduced. Thus, in contrast to other perceptual phenomena the visual neural mechanisms underlying the generation of express saccades are not affected by isoluminance nor low contrast luminance.

Reduction of blood flow to the rat retina was achieved by either clamping both carotid arteries briefly (24 min) or combining clamping of the carotid arteries with permanent occlusion of the vertebral arteries. Analysis of retinas 6 days after operations showed that GFAP immunoreactivity is expressed throughout the retinal Müller cells, although this was variable in retinas from animals where only the carotid arteries were clamped. GFAP immunoreactivity was not associated with retinal Müller cells from control animals and no obvious neuronal damage was observed in retinas from operated animals. These data suggest that Müller-cell GFAP expression may be used as an index to follow possible processes leading to an ischemic insult.

Different techniques were used to manipulate the inhibitory interaction between the red and green photoreceptors (R and G cones) of rhesus and human primates. The response techniques that were used were the corneal electroretinogram (ERG) and psychophysical increment-threshold spectral sensitivity functions. Red-green opponency, as measured by the depth of the notch at 580 nm, is removed by intravitreal injection of bicuculline but not by strychnine. Therefore, red-green opponency is mediated by GABA and not glycine. The depth of the notch is dependent upon stimulus size. Between 30' and 15' test light diameters, this sign of red-green opponency disappears. Psychophysical increment thresholds are shown to produce the notch while decrements do not and intravitreal APB is shown to reduce the notch, evidence that red-green opponency is carried by the “ON” and not the “OFF” bipolar pathways of the retina. Red and green annuli are shown to selectively reduce red and green inhibition, as though there were selective reduction of the surround response in center-surround organized red-green receptive fields.

Dopamine exerts multiple effects on retinal horizontal cells. Dopamine, via cyclic AMP and protein kinase A, reduces the light responsiveness of horizontal cells and the electrical coupling between the cells. The gating kinetics of both gap-junctional and glutamate channels are altered as a result of phosphorylation by protein kinase A. Dopamine also causes a reversible retraction of neurites of horizontal cells maintained in culture. Diacylglycerol analogues as well as phorbol esters mimic this effect of dopamine, but not cyclic AMP analogues or Forskolin. The results suggest that dopamine causes neurite retraction by the activation of protein kinase C via diacylglycerol.