The functions of the primate color-opponent and broad-band channels were assessed by examining the visual capacities of rhesus monkeys following selective lesions of parvocellular and magnocellular lateral geniculate nucleus, which respectively relay these two channels to the cortex. Parvocellular lesions impaired color vision, high spatial-frequency form vision, and fine stereopsis. Magnocellular lesions impaired high temporal- frequency flicker and motion perception but produced no deficits in stereopsis. Low spatial-frequency form vision, stereopsis, and brightness perception were unaffected by either lesion. Much as the rods and cones of the retina can be thought of as extending the range of vision in the intensity domain, we propose that the color-opponent channel extends visual capacities in the wavelength and spatial-frequency domains whereas the broad-band channel extends them in the temporal domain.

Ibotenic-acid lesions of the magnocelluar portion of the macaque lateral geniculate nucleus were used to examine the role of the M-cell pathway in spatio-temporal contrast sensitivity. A lesion was place in layer 1 of the lateral geniculate of each of two monkeys. Physiological mapping in one animal demonstrated that the visual-field locus of the lesion was on the horizontal meridian, approximately 6 deg in the temporal field. Visual thresholds were tested monocularly in the contralateral eye, and fixation locus was monitored with a scleral search coil to control the retinal location of the test target.

Three threshold measures were clearly disrupted by the magnocellular lesions. Contrast sensitivity for a 1 cycle/deg grating that drifted at 10 Hz was reduced from about twofold greater than, to about the same as, that for 10-Hz counterphase modulated gratings. Sensitivity for a very low spatial frequency (Gaussian blob), 10-Hz flickering stimulus was reduced so severely that no threshold could be measured. In addition, flicker resolution was greatly reduced at lower modulation depths (0.22), but not at higher depths (1.0). Two of the measured thresholds were unaffected by the lesions. Contrast sensitivity for 2 cycle/deg stationary gratings remained intact, and little or no effect on sensitivity was found for 1 cycle/deg, 10-Hz counterphase modulated gratings.

Together, these results suggest that the magnocellular pathway makes little contribution to visual sensitivity at low to moderate temporal frequencies. On the other hand, some contribution to detection sensitivity is evident at lower spatial and high temporal frequencies, especially for drifting stimuli. It appears that a major role of the magnocellular pathway may be to provide input to cortical mechanisms sensitive to rapid visual motion.

A series of psychophysical tests examining early and later aspects of image-motion processing were conducted in a patient with bilateral lesions involving the posterior visual pathways, affecting the lateral parietal-temporal-occipital cortex and the underlying white matter (as shown by magnetic resonance imaging studies and confirmed by neuro-ophthalmological and neuropsychological examinations). Visual acuity, form discrimination, color, and contrast-sensitivity discrimination were normal whereas spatial localization, line bisection, depth, and binocular stereopsis were severely impaired. Performance on early motion tasks was very poor. These include seeing coherent motion in random noise (Newsome & Paré, 1988), speed discrimination, and seeing two-dimensional form from relative speed of motion. However, on higher-order motion tasks the patient was able to identify actions from the evolving pattern of dots placed at the joints of a human actor (Johansson, 1973) as well as discriminating three-dimensional structure of a cylinder from motion in a dynamic random-dot field. The pattern of these results is at odds with the hypothesis that precise metrical comparison of early motion measurements is necessary for higher-order “structure from motion” tasks.

Using an antibody against serotonin (5-hydroxytryptamine, 5-HT), serotonin-like immunoreactive (serotonin IR) neurons were demonstrated in the retina of adult Bufo marinus. All immunoreactive neurons were identified as amacrine cells (ACs). The dendrites of serotonin-IR ACs branched diffusely and densely throughout all levels of the inner plexiform layer (IPL) of the retina. The great majority of these cell somata were located in the vitread part of the inner nuclear layer (INL) and a few of them (ranging from 9–29 cells) were displaced into the ganglion cell layer (GCL). On the basis of the soma sizes, two populations of serotonin-IR ACs, large (type A) and small (type B), were distinguished. 6-Hydroxydopamine (6-OHDA) injected into the eye abolished immunoreactivity in the recently reported tyrosine hydroxylase (TH)-IR ACs (Zhu & Straznicky, 1990), whereas serotonin-IR ACs remained unaffected.

The number of serotonin-IR cells per retina ranged from 23,750–27,390, with a ratio of 1:1.6 to 1:1.9 between type A and B cells. Both cell types were distributed nonuniformly across the retina. Cell densities were slightly lower in the peripheral (96 cells/mm2) than in the central (164 cells/mm2) retina. Linear regression analysis confirmed the presence of a decreasing density gradient from the retinal center to the retinal margin for both small and large cell types. The analysis of the nearest neighbor distances showed that the retinal distribution of serotonin-IR ACs was orderly.

These results have been taken to indicate that 5-HT-IR cells correspond to a population of serotonincontaining ACs. It is suggested that dopamine and serotonin are contained in two different populations of ACs in the rtina of Bufo marinus.

An eletrical potential recorded from the cornea, the a-wave of the ERG, is evaluated as a measure of human photoreceptor activity by comparing its behavior to a model derived from in vitro recordings from rod photoreceptors. The leading edge of the ERG exhibits both the linear and nonlinear behavior perdicted by this model. The capability for recording the electrical activity of humans photoreceptors in in vivo opens new avenues for assessing normal and abnormal receptor activity in humans. Furthermore, the quantitative model of the receptor response can be used to isolate the inner retinal contribution, Granit's PII, to the gross ERG. Based on this analysis, the practice of using the trough-to-peak amplitude of the b-wave as a proxy for the amplitude of the inner nuclear layer activity is evaluated.

Ganglion cells in the albino rat retina were retrogradely labeled with the fluorescent dye, diamidino-yellow, from the superior colliculus. Preembedding and postembedding immunocytochemical techniques were employed in conjunction with computer-assisted image processing to visualize SP- and GABA-immunoreactivity. Examination of flatmount and sectioned retinas revealed that approximately 3% of the ganglion cells projecting to the contralateral superior colliculus exhibit SP-immunoreactivity. Moreover, these cells were found to comprise a subpopulation of the GABA-immunoreactive cells projecting to the rat tectum.

The cellular connectivity of the lacertilian parietal eye is not well understood. Because the intercellular connections establish the foundation for information processing, we have investigated cellular connectivity of one cell type in this simple vertebrate retina. We also developed an in vitro preparation to study the anatomy of the parietal eye visual system. Horseradish peroxidase transport in the in vitro preparation revealed a class of displaced ganglion cells occupying positions among the photoreceptors, in a location where the presence of interneurons had been suggested. Three-dimensional reconstruction at the electron-microscopic level showed that the morphology and synaptic input of these displaced ganglion cells is different from that of the previously known ganglion cells. The displaced ganglion cells receive an average of about 13 ribbon synapses from photoreceptors. The ribbon input is equally distributed between the soma and dendritic arbor. Junctional membrane measurement and ethnolic phosphotungstic acid-staining provided evidence for the existence of non-ribbon synaptic contacts (synaptoid junctions). Displaced ganglion cells make about 20 synaptoid junctions, 65% of which are on the dendritic arbor. The morphology of the displaced ganglion cell is such that a significant measure of synaptic input to the dendritic arbor will be transmitted to the soma.

A role for endogenous dopamine in the control of rod and contributions to a second-order retinal neuron, the horizontal cell (HC) was studied in the Xenopus retina. Relative rod and cone contributions were estimated from HC responses to scotopically balanced 491- and 650-nm flashes. In eyecups prepared in light then placed in darkness, cone input to the HC slowed and diminished on a time scale of hours. The decline in cone input was balanced by a slow growth of rod input to the HC. Administration of D-amphetamine, a dopamine releasing agent, restored the light-adapted waveform.

The kinetics of slow light adaptation were examined by recording HC responses from eyecups that had been dark-adapted previously for 11–14 h. When test flashes fell on a dark field, cone input to the HC grew for 2–4 h, reached a plateau, and later declined. If, however, flashes were superimposed on a weak background field, cone input to the HC continued to increase monotonically at about 10%/h. This increase was abolished by superfusion with a nonspecific dopamine receptor blocker, cis-flupenthixol (50 μM), resulting in the complete suppression of cone-to-horizontal cell synaptic transfer and the enhancement of rod-to-horizontal cell communication. Subcutaneous injection of reserpine, a drug that depletes dopamine stores (2 mg/kg on 1–4 successive days), or intraocular injection of the dopamine neurotoxin, 6-hydroxydopamine (10–30 μg) slowed and reduced the amplitude of cone input to the HC, even in completely light-adapted eyes. Subsequent treatment with D-amphetamine (5–50 μM) or dopamine (10 μM) partially restored the normal response.

Our experimental findings are consistent with the following hypothesis. Weak light is sufficient to stimulate dopamine release; dopamine augments cone-to-horizontal cell synaptic transfer and reduces rod-to-horizontal cell communication. The rapid kinetics of the fully light-adapted response depend on the presence of dopamine. Thus, dopamine appears to be an intraretinal signal for slow light adaptation.