In the vertebrate retina, vision is initiated and maintained by the photolysis and regeneration, respectively, of light-sensitive pigments in the disk membranes of the photoreceptor outer segments. This cyclical process depends on an exchange of retinoids between the photoreceptors and the retinal pigment epithelium (RPE). There is a great deal of indirect evidence that the transport of retinoids between these cellular compartments is mediated by the interphotoreceptor retinoid-binding protein (IRBP), a large glycoprotein synthesized in the photoreceptors and extruded into the interphotoreceptor matrix (IPM) that fills the subretinal space. Nevertheless, a number of in vitro experiments have demonstrated that an intermembranous transfer of retinoids can occur through an aqueous medium independent of any retinoid-binding protein. This led to the suggestion that IRBP may play the more passive role of an extracellular buffer, serving to prevent the degradation and potentially cytotoxic effects of free retinoids when large amounts are released into the IPM. We have studied the structural and functional properties of transgenic mice in which homologous recombination was used to delete the IRBP gene. Light- and electron-microscopic examination of the retinas of “knockout” (IRBP−/−) mice revealed a significant loss of photoreceptor nuclei, and profound changes in the structure and organization of the receptor outer segments. Consistent with these observations, electroretinographic recordings showed a marked reduction in response amplitude for both rod- and cone-mediated potentials. However, despite the histological and electrophysiological changes, there was no evidence of gross abnormalities in the visual cycle. After bleaching a significant fraction of the available rhodopsin, electroretinogram amplitude and rhodopsin density gradually increased toward their pre-bleach levels, and the rates of recovery were even more rapid than those seen in wild-type (IRBP+/+) mice.

Subtypes of bipolar cells were identified by protein kinase C (PKC)-like immunoreactivity in the goldfish retina. The PKC-like immunoreactivity was visualized by either the avidin/biotin peroxidase method or immunofluorescence method. In frozen cross sections and in wholemounts, the monoclonal antibody against α species of PKC reacted with ON-type bipolar cells, identified by the location of axon terminals in sublamina b of the inner plexiform layer. OFF-type bipolar cells (identified by the location of the axon terminal in sublamina a of the inner plexiform layer) were not immunoreactive. The immunoreactive cells consisted of two subtypes; the rod-dominant ON-type with a large soma and a large bulbous axon terminal, and the cone-dominant ON-type with a small soma and small axon terminal. Antibodies against β and γ species of PKC did not react with any bipolar cells. Of the isolated bipolar cells, enzymatically dissociated from the goldfish retina, 59% were immunoreactive to the monoclonal antibody against α species of PKC. The immunoreactive isolated cells also consisted of two morphological types. Each of them had a morphology typical either to rod-dominant ON-type or to cone-dominant ON-type.

The Jackson Laboratory, having the world's largest collection of mouse mutant stocks and genetically diverse inbred strains, is an ideal place to discover genetically determined eye variations and disorders. In this paper, we list and describe mouse models for ocular research available from Mouse Eye Mutant Resource at The Jackson Laboratory. While screening mouse strains and stocks at The Jackson Laboratory (TJL) for genetic mouse models of human ocular disorders, we have identified numerous spontaneous or naturally occurring mutants. We characterized these mutants using serial indirect ophthalmoscopy, fundus photography, electroretinography (ERG) and histology, and performed genetic analysis including linkage studies and gene identification. Utilizing ophthalmoscopy, electroretinography, and histology, to date we have discovered 109 new disorders affecting all aspects of the eye including the lid, cornea, iris, lens, and retina, resulting in corneal disorders, glaucoma, cataracts, and retinal degenerations. The number of known serious or disabling eye diseases in humans is large and affects millions of people each year. Yet research on these diseases frequently is limited by the obvious restrictions on studying pathophysiologic processes in the human eye. Likewise, many human ocular diseases are genetic in origin, but appropriate families often are not readily available for genetic studies. Mouse models of inherited ocular disease provide powerful tools for rapid genetic analysis, characterization, and gene identification. Because of the great similarity among mammalian genomes, these findings in mice have direct relevance to the homologous human conditions.

The nonretinotopic portion of the macaque pulvinar complex is interconnected with the occipitoparietal and occipitotemporal transcortical visual systems where information about the location and motion of a visual object or its form and color are modulated by eye movements and attention. We recorded from single cells in and about the border of the dorsal portion of the lateral pulvinar and the adjacent medial pulvinar of awake behaving Macaca mulatta in order to determine how the properties of these two functionally dichotomous cortical systems were represented. We found a class of pulvinar neurons that responded differentially to ten different patterns or broadband wavelengths (colors). Thirty-four percent of cells tested responded to the presentation of at least one of the pattern or color stimuli. These cells often discharged to several of the patterns or colors, but responded best to only one or two of them, and 86% were found to have statistically significant pattern and/or color preferences. Pattern/color preferential cells had an average latency of 79.1 ± 46.0 ms (range 31–186 ms), responding well before most inferotemporal cortical cell responses. Visually guided and memory-guided saccade tasks showed that 58% of pattern/color preferential cells also had saccade-related properties e.g. directional presaccadic and postsaccadic discharges, and inhibition of activity during the saccade. In the pulvinar, the mean presaccadic response latency was earlier, and the mean postsaccadic response latency was later, than those reported for parietal cortex. We also discovered that the strength of response to patterns or colors changed depending upon the behavioral setting. In comparison to trials in which the monkey fixated dead ahead during passive presentations of pattern and color stimuli, 92% of the cells showed attenuated responses to the same passive presentation of patterns and colors during fixation when these trials were interleaved with trials which also required active saccades to pattern and color targets in the periphery. We conclude that properties which represent the functionally dichotomous object and spatial visual systems are found together in single pulvinar neurons and that the responses of these cells to pattern or color stimuli are influenced by the focus of spatial attention. The pulvinar is the first structure in the brain shown to have neurons which integrate both object and spatial properties and the response latencies indicate that this information is processed before that in cortex. These results are discussed in terms of role of the pulvinar in visual attention as well as its unique role in providing both object feature and spatial location information to the inferotemporal cortex.

We have studied the responses of striate cortical neurons to stimuli whose contrast is modulated in time by either a single sinusoid or by the sum of eight sinusoids. The sum-of-sinusoids stimulus resembles white noise and has been used to study the linear and nonlinear dynamics of retinal ganglion cells (Victor et al., 1977). In cortical neurons, we have found different linear and second-order responses to single-sinusoid and sum-of-sinusoids inputs. Specifically, while the responsivity near the optimal temporal frequency is lower for the sum-of-sinusoids stimulus, the responsivity at higher temporal frequencies is relatively greater. Along with this change in the response amplitudes, there is a systematic change in the time course of responses. For complex cells, the integration time, the effective delay due to a combination of actual delays and low-pass filter stages, changes from a median of 85 ms with single sinusoids to 57 ms with a sum of sinusoids. For simple cells, the integration times for single sinusoids range from 44–100 ms, but cluster tightly around 40 ms for the sum-of-sinusoids stimulus. The change in time constant would argue that the increased sensitivity to high frequencies cannot be explained by a static threshold, but must be caused by a fundamental alteration in the response dynamics. These effects are not seen in the retina (Shapley & Victor, 1981) and are most likely cortical in origin.

The receptive field (RF) of most retinal ganglion cells (RGCs) is comprised of an excitatory center and an antagonistic surround. Interactions between these RF elements shape most of the visual responses of RGCs. To begin to investigate center-surround interactions of mouse RGCs quantitatively, we characterized their responses in an in vivo preparation to a variety of spot and full-field stimuli. When RGCs were stimulated with a spot that matched the cell's RF center diameter (optimal spot), all RGCs could be categorized as either ON- or OFF-center. In all RGCs, full-field stimulation significantly reduced both the peak and the mean firing rates evoked with an optimal spot stimulus. Full-field stimulation revealed differences in other response properties between ON- and OFF-center RGCs. With a full-field stimulus, the duration of the OFF-center RGCs response was reduced making them more transient, while the duration of the ON-center RGCs increased making them more sustained. Of most interest, full-field stimulation altered the RF center response sign in approximately half of the OFF-center RGCs, which became either OFF/ON or ON only. In contrast, all ON-center and the other OFF-center cells conserved their RF response sign in the presence of the full-field stimulus. We propose that sign-altering OFF-center RGCs possess an additional RF surround mechanism that underlies this alteration in their response. Of general interest these results suggest that the sole use of full-field stimulation to categorize visual response properties of RGCs does not adequately reflect their RF organization and, therefore, is not an optimal strategy for their classification.

Cells in area V1 of the anesthetized macaque monkey were stimulated with large texture patterns composed of homogeneous regions of line elements (texels) with different orientations. To human observers, such patterns appear to segregate, with the percept of sharp boundaries between texture regions. Our objective was to investigate whether the boundaries are reflected in the responses of single cells in V1. We measured responses to individual texels at different distances from the texture border. For each cell, patterns of optimally or orthogonally orientated texels were adjusted so that only one texel fell into the receptive field and all other texels fell in the visually unresponsive regions outside. In 37 out of 156 neurons tested (24%), texels immediately adjacent to a texture border evoked reliably larger responses than identical texels farther away from the border. In 17 neurons (11%), responses to texels near the border were relatively reduced. Border enhancement effects were generally stronger than border attenuation effects. When tested with four different border configurations (two global orientations and two edge polarities), many cells showed reliable effects for only one or two configurations, consistent with cells encoding information about the orientation of the texture border or its location with respect to the segmented region. Across the sample, enhancement effects were similar for all texture borders. Modulation by the texture surround was predominantly suppressive; even the responses near texture borders were smaller than those to a single line. We compared these results with the results of a popout test in which the line in the receptive field was surrounded by homogeneous texture fields either orthogonal or parallel to the center line. The patterns of response modulation and the temporal onset of differential responses were similar in the two tests, suggesting that the two perceptual phenomena are mediated by similar neural mechanisms.

γ-aminobutyric acid (GABA) has been reported to be an important neurotransmitter in the retinas of many species. This immunocytochemical study detailed the localization of antigens resembling GABA and glutamic acid decarboxylase (GAD, an enzyme involved in the synthesis of GABA), in retinal neurons in the turtle, Pseudemys scripta elegans. GABA-like immunoreactivity was present within somata in the inner and outer regions of the inner nuclear layer, within somata in the ganglion cell layer, and in processes in the outer plexiform layer, inner plexiform layer, and ganglion cell axon layer. GAD-like immunoreactivity was found in somata in the inner and outer regions of the inner nuclear layer and in processes in the inner and outer plexiform layers. Cell counts indicated more somata with GABA-like than GAD-like immunoreactivity in the inner nuclear layer. Double-label studies showed that every somata in the inner nuclear layer which had GAD-like immunoreactivity also had GABA-like immunoreactivity, but that many somata had only GABA-like immunoreactivity.

The stratification of immunoreactivity within the inner plexiform layer was analyzed using a scanning densitometer. We described the strata within the inner plexiform layer such that S0 represented the inner nuclear layer/inner plexiform layer border and S100 represented the inner plexiform layer/ganglion cell layer border. Analysis of GAD-like labeling yielded seven distinct strata with peak densities at positions S8, S19, S28, S42, S59, S75, and S93. GABA-like labeling provided five distinct strata with peak densities at positions S17, S28, S67, S84, and S95. The strata with peaks of GABA-like immunoreactivity at S17 and S28 were in statistically identical locations to corresponding strata with GAD-like immunoreactivity. The strata with GABA-like immunoreactivity at S67, S84, and S95 did not have statistically identical peaks of correlated GAD-like immunoreactivity, although there were corresponding strata with GAD-like immunoreactivity nearby. Antiserum directed against GABA failed to produce labeled strata at positions corresponding to the strata with GAD-like immunoreactivity at S8 and S42.

In summary, our results indicated that the antisera we used, which were directed against GABA and GAD, produced significantly different labeling in the inner nuclear layer, inner plexiform layer, and the ganglion cell body and axon layers of the turtle retina. Until the physiological significance of these differences is resolved, studies employing these markers to investigate the function of GABA in the turtle retina should be interpreted with caution.

We have studied, by immunocytochemistry, the ontogeny of GABA, glycine, glutamate, glutamine, and taurine-containing cells in the rabbit retina. Amacrine cells show GABA immunoreactivity by embryonic day 25 (E25) and throughout postnatal life. By contrast, ganglion cells and horizontal cells are only transiently GABA-immunoreactive (-IR); few appear GABA-IR by the third postnatal week. At maturity, glycine is present in amacrine cells and in some bipolar cells. During development, putative ganglion cells transiently contained glycine between E25 and postnatal day 3 (P3), whereas immunolabelling in presumed amacrine cells and bipolar cells persists after birth. Ganglion cells, bipolar cells, photoreceptors, and some amacrine cells are glutamate-IR in the adult retina. Glutamate immunoreactivity first appears in the somata and processes of cytoblastic cells by E20 and is prominent by E25. Surprisingly, ganglion cells are not strongly glutamate-IR until just before eye-opening, at postnatal day 10 (P10), coincident with the appearance of glutamine in their somata and in Müller glial cells. Bipolar cells are glutamate-IR before they or Müller cells contain high levels of glutamine (at P10). Glutamate immunoreactivity in photoreceptors is progressively restricted to the inner segments by eye-opening. At no stage are presumed horizontal cells glutamate-IR or glutamine-IR, but some amacrine cells show glutamate- and glutamine-IR by P10. Taurine is localized to photoreceptors and Müller glial in the adult retina. Some cytoblasts are taurine-IR at E20; with ensuing development, taurine labelling becomes restricted primarily to Müller cells and photoreceptors; some putative bipolar cells may also be labelled. However, for a few days around birth, cells resembling horizontal cells, also show taurine immunoreactivity. The early appearance and often transient expression of these amino acids in retinal cells suggests that these neuroactive molecules may be involved in the structural and functional development of the retina.

We examined the distribution and morphological types of ganglion cells in the retina of the zebrafish, a model vertebrate genetic organism. Using cresyl violet and methylene blue staining, a prominent central area was observed in the ventral temporal retina. The density of ganglion cell layer neurons averaged from ∼12,000/mm2 in the dorsal-nasal retina to a peak of ∼37,000/mm2 in the ventral-temporal retina. Individual zebrafish ganglion cells were labeled by backfilling with DiI through the optic nerve followed by reconstruction using confocal microscopy. The dendritic stratification and branching pattern of each labeled ganglion cell was examined in relation to the borders of the inner plexiform layer (IPL). We identified 11 different morphological types of ganglion cell. The most commonly labeled ganglion cells were two types termed Type III or IV, which displayed highly stratified dendritic arborizations in their respective ON-, OFF-sublaminae of the IPL. Their dendritic branching patterns were highly asymmetric with many thorn-like varicosities that profusely filled the area of arborization. In contrast, Type V cells formed a small simply branching dendritic field in the innermost portion of the ON-sublamina of the IPL. Two large ganglion cell types (Types I and II) with wide monostratified dendritic fields were found in both the ON- and OFF-sublamina of the IPL. Three different types of multistratified/bistratified ganglion cells were found (Types, IX, X, and XI.) whose dendrites occupied different regions of the IPL. The multistratified dendrites of IX cells occupied the whole width of the IPL, while the dendrites of Type XI cells formed vertical claw-like endings in only the ON-sublamina of the IPL. We conclude that zebrafish ganglion cells display a rich variety of types and branching patterns. This study establishes a series of baseline measurements of zebrafish ganglion cells to facilitate examination of genes playing a role in the specification and stratification of ganglion cell types.

Eye growth and refraction are regulated by visual processing in the retina. Until now, the messengers released by the retina to induce these changes are largely unknown. Previously, it was found that glucagon amacrine cells respond to defocus in the retinal image and even to its sign. The expression of the immediate-early gene product ZENK increased in this cell population in eyes wearing plus lenses and decreased in minus lens-treated chicks. Moreover, it was shown that the amount of retinal glucagon mRNA increased during treatment with positive lenses. Therefore, it seems likely that these cells contribute to the visual regulation of ocular growth and that glucagon may act as a stop signal for eye growth. The purpose of the present study was to accumulate further evidence for a role of glucagon in the visual control of eye growth. Chicks were treated with plus and minus lenses after injection of different amounts of the glucagon antagonist des-His1-Glu9-glucagon-amide or the agonist Lys17,18,Glu21-glucagon, respectively. Refractive development and eye growth were recorded by automated infrared photorefraction and A-scan ultrasound, respectively. The glucagon antagonist inhibited hyperopia development, albeit only in a narrow concentration range, and at most by 50%, but not myopia development. In contrast, the agonist inhibited myopia development in a dose-dependent fashion. At high concentrations, it also prevented hyperopia development.

The distribution of ganglion cells in the retina of the silver lamprey, Ichthyomyzon unicuspis, was revealed by retrograde labeling from the optic nerve with horseradish peroxidase (HRP) and fluorescent-labeled dextrans in live animals and with the fluorescent dye DiI in aldehyde-fixed tissue. The majority of ganglion cells (74%) termed the “outer ganglion cells,” are multipolar and are located at the vitread boundary of the inner nuclear layer. The remaining ganglion cells (26%), termed the “inner ganglion cells” are bipolar and are distributed in a sublamina within the inner plexiform layer. The dense, dendritic meshwork of the outer ganglion cells is largely restricted to the sclerad half of the inner plexiform layer with some cells possessing dendrites which pass through the inner nuclear layer to terminate within the outer plexiform layer. The dendrites of the inner ganglion cells form a thin, dendritic network apposing the inner limiting membrane. Axons from both populations of ganglion cells originate from dendrites or the soma and form fascicles lying adjacent to the outer ganglion cell somata.

Retinopetal fibers, originating from bilaterally distributed neurons of the tegmental midbrain, were thin and varicose and ran parallel to the ganglion cell axons to terminate either with a varicose enlargement or a few short sidebranches in the sclerad third of the inner plexiform layer. The unusual organization of the lamprey retina and outgroup comparison with hagfish suggests that agnathans share a presumably primitive type of retinal ganglion cell organization compared to that of gnathostomes.

Over the last 50 years, studies of receptive fields in the early mammalian visual system have identified many classes of response properties in brain areas such as retina, lateral geniculate nucleus (LGN), and primary visual cortex (V1). Recently, there has been significant interest in understanding the cellular and network mechanisms that underlie these visual responses and their functional architecture. Small mammals like rodents offer many advantages for such studies, because they are appropriate for a wide variety of experimental techniques. However, the traditional rodent models, mice and rats, do not rely heavily on vision and have small visual brain areas. Squirrels are highly visual rodents that may be excellent model preparations for understanding mechanisms of function and disease in the human visual system. They use vision for navigating in their environment, predator avoidance, and foraging for food. Visual brain areas such as LGN, V1, superior colliculus, and pulvinar are particularly large and well elaborated in the squirrel, and the squirrel has several extrastriate cortical areas lateral to V1. Unlike many mammals, most squirrel species are diurnal with cone-dominated retinas, similar to the primate fovea, and have excellent dichromatic color vision that is mediated by green and blue cones. Owing to their larger size, squirrels are physiologically more robust than mice and rats under anesthesia, and some hibernating species are particularly tolerant of hypoxia that occurs during procedures such as brain slicing. Finally, many basic anatomical and physiological properties in the early visual system of squirrel have now been described, permitting investigations of cellular mechanisms. In this article, we review four decades of anatomical, behavioral, and physiological studies in squirrel and make comparisons with other species.

In the present study, the anterograde tracer Phaseolus vulgaris-leucoagglutinin was injected into area V1 in order to demonstrate the detailed morphology of individual axons terminating in prestriate area MT. On the basis of 24 axon reconstructions, several representative (but not necessarily comprehensive) characteristics have been identified: (1) Most axons arborize in a patchy manner over a widespread territory, frequently greater than 1.0 mm and often up to 1.5 × 1.8 mm (dimensions uncorrected for shrinkage). (2) Terminal arbors are distributed to layers 3, 4, and 6. Those in layer 6 need not be in register with those in the upper layers. (3) Number and size of terminal arbors are variable. One axon may have 1–4 arbors in the middle layers; typically at least one of these will have a diameter of 200–250 µm, while the others may be less developed. There are from 1–3 arbors in layer 6, usually 50 µm (but sometimes up to 100 µm) in diameter. (4) Terminal boutons are of mixed morphology, but usually beaded and large (up to 3.0 µm). (5) In the white matter, many axons travel in the external sagittal stratum but some are part of the U-fiber system. Axons commonly branch, sometimes at depths up to 0.75–1.0 mm, below the gray matter of MT. In summary, these axons are not stereotyped, but rather vary in the number and size of their terminal arbors, as well as in their branching and overall geometry.

Connections from area V1 to MT have been associated with the magnocellular-dominated “processing channel.” As widespread arborizations and bistratified terminations are common to both striate axons in MT and to geniculocortical axons in layer 4Cα of primary visual cortex, these features might be correlated with magnocellular-specific processing requirements.

Following bright flashes, rod photoreceptors exhibit a period of photocurrent saturation that increases linearly with the logarithm of flash intensity. In a recent report, Pepperberg et al. (1992) presented evidence that the slope of the function relating the saturation period (T) to the natural logarithm of flash intensity (In If) represents the exponential lifetime (τ) of photoactivated visual pigment: τ = ΔT/Δ[ln If]. In salamander rods, 11 -cis 9-desmethylretinal combines with opsin to form 9-desmethyl rhodopsin. Dim flash responses mediated by this analogue visual pigment exhibited slow recovery kinetics relative to those of native pigment (Corson et al., 1991). This observation raises the hypothesis that the physiological lifetime of photoactivated 9-desmethyl rhodopsin is substantially longer than that of native visual pigment. To test this hypothesis, we have examined the relation between the period of photocurrent saturation and flash intensity in salamander rods containing a mixture of the two pigments. Brief stimuli at two widely separated wavelengths (440 and 640 nm) elicited saturating photocurrent responses that were preferentially mediated by 9-desmethyl rhodopsin or residual native pigment, respectively. Plots of T vs. In If revealed a linear increase in the period of response saturation over a large range of saturating intensities at both wavelengths. However, the slope of the relation between T and In If with 440-nm flashes was more than twice as large (4.1 ± 0.5 s, n = 5) as that measured with 640-nm flashes (1.7 ± 0.4 s). For rods subjected only to bleaching of the native pigment, or to bleaching and resensitization with 11-cis retinal, the slope of the relation between T and In If remained independent of wavelength and indistinguishable from that of native pigment in unbleached cells. The data provide support for the hypothesis that the slope parameter τ represents the lifetime of photoactivated pigment, and specifically suggest that the lifetime of photoactivated 9-desmethyl rhodopsin is abnormally long.

We studied the effect of cooling the striate cortex on parvocellular lateral geniculate nucleus (PLGN) neurons in awake monkeys. Cooling the striate cortex produced both facilitation and inhibition of the responses of all neurons, depending on the stimulus presented. Cooling the striate cortex also altered the temporal distribution of spikes in the responses of PLGN neurons. Shannon's information measure revealed that cooling the striate cortex reduced the average stimulus-related information transmitted by all PLGN neurons. The reduction in transmitted information was associated with both facilitation and inhibition of the response. Cooling the striate cortex reduced the amount of information transmitted about all of the stimulus parameters tested: pattern, luminance, spatial contrast, and sequential contrast. The effect of cooling was nearly the same for codes based on the number of spikes in the response as for codes based on their temporal distribution. The reduction in transmitted information occurred because the differences among the responses to different stimuli (signal separation) were reduced, not because the variability of the responses to individual stimuli (noise) was increased. We conclude that one function of corticogeniculate feedback is to improve the ability of PLGN neurons to discriminate among stimuli by enhancing the differences among their responses.

The perceived direction of a grating moving behind an elongated aperture is biased towards the aperture's long axis. This “barber pole” illusion is a consequence of integrating one-dimensional (1D) or grating and two-dimensional (2D) or terminator motion signals. In humans, we recorded the ocular following responses to this stimulus. Tracking was always initiated at ultra-short latencies (≈ 85 ms) in the direction of grating motion. With elongated apertures, a later component was initiated 15–20 ms later in the direction of the terminator motion signals along the aperture's long axis. Amplitude of the later component was dependent upon the aperture's aspect ratio. Mean tracking direction at the end of the trial (135–175 ms after stimulus onset) was between the directions of the vector sum computed by integrating either terminator motion signals only or both grating and terminator motion signals. Introducing an elongated mask at the center of the “barber pole” did not affect the latency difference between early and later components, indicating that this latency shift was not due to foveal versus peripheral locations of 1D and 2D motion signals. Increasing the size of the foveal mask up to 90% of the stimulus area selectively reduced the strength of the grating motion signals and, consequently, the amplitude of the early component. Conversely, reducing the contrast of, or indenting the aperture's edges, selectively reduced the strength of terminator motion signals and, consequently, the amplitude of the later component. Latencies were never affected by these manipulations. These results tease apart an early component of tracking responses, driven by the grating motion signals and a later component, driven by the line-endings moving at the intersection between grating and aperture's borders. These results support the hypothesis of a parallel processing of 1D and 2D motion signals with different temporal dynamics.

The lateral geniculate nucleus (LGN) of primates contains three classes of relay cells, the magnocellular (M), parvocellular (P), and koniocellular (K) cells. At present, very little is known about either the structure or function of the K relay cells in New or Old World monkeys (simian primates). In monkeys, K cells are located between the main LGN layers and adjacent to the optic tract. For convenience, these intercalated cell layers are numbered K1-K4 starting closest to the optic tract with K1. The objective of this study was to examine the details of K axon morphology in the primary visual cortex (V1) of owl monkeys and to determine if different K layers give rise to distinct axon types. For this purpose, injections of WGA-HRP or PHA-L were made into specific K LGN layers and the distribution and morphology of the resulting labeled axons were analyzed. Injections of fluorescent tracers also were made within the superficial layers of V1 to further document connections via analysis of the patterns of retrogradely labeled cells in the LGN. Our main finding is that K axons in owl monkeys terminate as delicate focused arbors within single cytochrome oxidase (CO) blob columns in cortical layer III and within cortical layer I. Overall, the morphology of the K axons in these monkeys is quite similar to what we described previously for K geniculocortical axons in the distantly related bush baby (prosimian primate), suggesting that the basic features of this pathway are common to all primates. Our results also provide evidence that the axon arbors from different K layers are morphologically distinct; axons from LGN layer K1 project mainly to cortical layer I, while axons from LGN layer K3 chiefly terminate in cortical layer III. Taken together, these results imply that the basic features of axons within the K pathway are conserved across primates, and that the K axons from different K layers are likely to differ in function based upon their different morphologies.

Two morphological types of melanopsin-expressing ganglion cells have been described in primate retina. Both types show intrinsic light responses as well as rod- and cone-driven ON-type responses. Outer stratifying cells have their dendrites close to the inner nuclear layer (OFF sublamina); inner stratifying cells have their dendrites close to the ganglion cell layer (ON sublamina). Both inner and outer stratifying cells receive synaptic input via ribbon synapses, but the bipolar cell types providing this input have not been identified. Here, we addressed the question whether the diffuse (ON) cone bipolar type DB6 and/or rod bipolar cells contact melanopsin-expressing ganglion cells. Melanopsin containing ganglion cells in marmoset (Callithrix jacchus) and macaque (Macaca fascicularis) retinas were identified immunohistochemically; DB6 cells were labeled with antibodies against the carbohydrate epitope CD15, rod bipolar cells were labeled with antibodies against protein kinase C, and putative synapses between the two cells types were identified with antibodies against piccolo. For one inner cell, nearly all of the DB6 axon terminals that overlap with its dendrites in the two-dimensional space show areas of close contact. In vertical sections, the large majority of the areas of close contact also contain a synaptic punctum, suggesting that DB6 cells contact inner melanopsin cells. The output from DB6 cells accounts for about 30% of synapses onto inner melanopsin cells. Synaptic contacts between rod bipolar axons and inner dendrites were not observed. In the OFF sublamina, about 10% of the DB6 axons are closely associated with dendrites of outer cells, and in about a third of these areas, axonal en passant synapses are detected. This result suggests that DB6 cells may also provide input to outer melanopsin cells.

The role of excitatory amino acid (EAA) receptors in primate retinal ganglion cell function was analyzed in a superfused retina-eyecup preparation using single-unit, extracellular recording techniques. The effects of bath applied L-2–amino-4–phosphonobutyrate (APB), N-methyl-D-aspartate (NMDA), and non-NMDA EAA receptor agonists and antagonists were examined on the light-evoked responses and resting firing rates of ganglion cells. APB (30–100 μM) reduced or blocked the light-evoked responses and resting firing rates of all ON-center ganglion cells; higher doses of APB (100 μM) were required to block the light-evoked responses of ON-transient cells. In contrast, an increase in resting firing rates was observed when L-APB was applied to some OFF-center ganglion cells. The EAA agonists kainate (KA) (10–20 μM) and NMDA (200–350 μM) increased the firing rate of virtually all ganglion cells examined. Quisqualate (10–20 μM) increased firing in most cells, but occasionally (4/13 cases) produced inhibition. The NMDA antagonist D-amino-phosphono-heptanoic acid (D-AP7) (200–250 μM) reduced the light-evoked responses of ganglion cells by an average of 12% from control levels, while resting firing rates declined 37%. In the presence of D-AP7, the basic receptive-field characteristics of cells were not significantly altered. In contrast, two non-NMDA receptor antagonists, NBQX (2,3–Dihydroxy-6–nitro-7–sulfamoyl-benzo-(F)-quinoxalinedione) and DNQX (6,7–dinitro-quinoxaline-2,3–dione), produced substantial reductions in the light-evoked responses (82%) and resting firing rates (87%) of all ganglion cell classes. A striking observation in some neurons was the recovery of a persistent transient light-evoked response in the presence of NBQX. This NBQX-insensitive, light-evoked response was always blocked by adding D-AP7. Thus, neurotransmission from bipolar to ganglion cells in primates is mediated predominantly by non-NMDA EAA receptors, with NMDA receptors forming a minor component of the light-evoked response.