In retinal rods, light exposure decreases the total outer segment content of both cGMP and cAMP by about 50%. The functional role of the light-evoked change in cAMP is not known. It is postulated to trigger changes in the phosphorylation state of phosducin, a phosphoprotein that is phosphorylated in the dark by cAMP-dependent protein kinase (PKA) and dephosphorylated by basal phosphatase activity when PKA is inhibited by the light-evoked drop in cAMP. In biochemical studies, dephosphorylated phosducin binds to free βγ dimer of transducin (Tβγ) and prevents the regeneration of heterotrimeric transducin by blocking the re-association of the βγ and α subunits. Phosducin's interaction with Tβγ is blocked when it is phosphorylated on a single residue by PKA. To evaluate the effect of the light-evoked fall in cAMP, functionally intact isolated lizard rod outer segments were dialyzed in whole-cell voltage clamp with a standard internal solution and electrical light responses were recorded with and without adding cAMP to the dialysis solution. Since the total outer segment content of cAMP in darkness is ∼5 μM, internal dialysis with solution containing a much higher concentration (100 μM) of cAMP (or 8-bromo-cAMP) will overcome the effects of a light-evoked decrease in its concentration by keeping cAMP-dependent processes fully activated. Neither cyclic nucleotide had any influence on the generation, light sensitivity, recovery, or background adaptation of the flash response. These results also argue against the participation of phosducin in the sequence of events that are responsible for these aspects of rod function. This does not exclude the possibility of phosducin being involved in adaptation caused by higher light levels than used in the present study, that is, bleaching adaptation, or in light-dependent processes other than phototransduction.

Cannabinoid CB1 receptors are distributed throughout the CNS and interact with GABA, glutamate, and dopamine systems. Cannabinoids have effects on the visual system, some of which may have a retinal component, particularly the enhancement of photosensitivity. We used immunocytochemistry and whole-cell recording to study cannabinoids in the goldfish retina. Immunoblots of an antiserum against amino acids (1-14) of the rat CB1 receptor produced a single band in goldfish retina at about 70 kDa. Light microscope immunocytochemistry of CB1 receptor immunoreactivity (CB1R-IR) revealed intense staining of Müller cells and weaker staining of ON bipolar cells (verified with double labeling with PKC-IR) and the outer and inner plexiform layers. Ultrastructural analysis revealed that CB1R-IR was localized intracellularly as well as on the plasma membrane of photoreceptor terminals, bipolar cell terminals and, rarely, amacrine cell boutons. Membrane-associated CB1R-IR was restricted to cone pedicles at sites removed from the synaptic ribbon. Regarding bipolar cells, membrane-associated CB1R-IR was found at 93% of the synaptic terminals in sublamina b (ON-type) and only at 33% of the synaptic terminals in sublamina a (OFF-type). Whole-cell recordings from large ON-type Mb bipolar cells showed that the delayed rectifier (IK(V)) was rapidly and reversibly inhibited by 1 μM of the cannabinoid agonists CP 54490 and (+)-WIN 55212-2, effects blocked completely by the antagonist SR 141716A (1 μM). Inhibition of IK(V) in the Mb bipolar cells by cannabinoids should result in a more tonic ON response to increments of light. As such, cannabinoids may play a role in modulating the temporal aspects of signaling in the retina.

The cat's lateralis medialis-suprageniculate nuclear complex (LM-Sg) in the thalamus receives input from various brain regions such as the superior colliculus, brain stem, and spinal cord, as well as from visual association cortex. In a previous study, we demonstrated that LM-Sg receives cholinergic fibers from the pedunculopontine tegmental nucleus (PPT) and that cholinergic terminals make synaptic contacts with the dendrites of glutamatergic projection neurons and of GABAergic interneurons (Hoshino et al., 1997). In this study, we investigate the distribution and the organization of PPT terminals by means of a combined anterograde tracer (biotinylated dextran amine, BDA) and immunohistochemical methods. When stained by acetylcholinesterase (AChE), the LM-Sg is not uniformly immunoreactive, but rather is patchily labeled and shows a streaming type of reactivity. The tissue content appears high in enzyme activity in AChE-positive zones and is much lighter in activity in AChE-negative zones. We compared the synaptic organization between AChE-positive and AChE-negative portions of the LM-Sg in separate groups of electron-microscopic material: four types of vesicle containing profiles (RS, RL, F1, and PSD) as well as synaptic glomeruli were observed in this nucleus. Among these, the PSD profiles were observed more frequently in AChE-positive portions than in AChE-negative zones. Furthermore, the number of glomeruli was significantly higher in AChE-positive than in AChE-negative zones. Following the injection of BDA into PPT, labeled terminals within LM-Sg were rather more concentrated in the AChE-positive portion. Although the majority of PPT terminals made synaptic contacts with dendrites in the neuropil, a few terminals were involved in the synaptic glomeruli. The present results show that the synaptic organization is distinctly different between the AChE-positive and AChE-negative portions of LM-Sg. These results suggest that the AChE-positive portions of LM-Sg are relatively more involved in integrating information arising from a diverse set of inputs and processing that information within glomeruli in a complex manner than occurs in the AChE-negative portion of LM-Sg.

We have measured visual evoked potentials (VEPs) to luminance-modulated, square-wave alternating, 3-deg homogeneous disks for stimulus frequencies ranging from 1 Hz to 16.7 Hz. The aim of the study was to determine the range of frequencies at which we could reproduce the two-branched contrast-response (C-R) curves we had seen at 1 Hz (Valberg & Rudvin, 1997) and which we interpreted as magnocellular (MC) and parvocellular (PC) segregation. Low-contrast stimuli elicited relatively simple responses to luminance increments resulting in waveforms that may be the signatures of inputs from magnocellular channels to the visual cortex. At all frequencies, the C-R curves of the main waveforms were characterized by a steep slope at low contrasts and a leveling off at 10%–20% Michelson contrast. This was typically followed by an abrupt increase in slope at higher contrasts, giving a distinctive two-branched C-R curve. On the assumption that the low-contrast, high-gain branch reflects the responsivity of magnocellular-pathway inputs to the cortex, the high-contrast branch may be attributed to additional parvocellular activation. While a two-branched curve was maintained for frequencies up to 8 Hz, the high-contrast response was significantly compromised at 16.7 Hz, revealing a differential low-pass filtering. A model decomposing the measured VEP response into two separate C-R curves yielded a difference in sensitivity of the putative MC- and PC-mediated response that, when plotted as a function of frequency, followed a trend similar to that found for single cells. Due to temporal overlap of responses, the MC and PC contributions to the waveforms were hard to distinguish in the transient VEP. However, curves of time-to-peak (delay) as a function of contrast often went through a minimum before the high-contrast gain increase of the corresponding C-R curve, supporting the notion of a recruitment of new cell ensembles in the transition from low to high contrasts.

The photoreceptor layer of F. heteroclitus was examined by light and electron microscopy. We identified four cone visual pigments with maximum absorbance (λmax) in the UV (363 nm), short (400 nm), middle (463 nm), and long (563 nm) wavelength regions of the spectrum and a rod visual pigment that peaked in the middle wavelengths (503 nm). Electron-dense bodies, ellipsosomes and pseudoellipsosomes, were present in the distal ellipsoids of long/middle (L/M) and long/long (L/L) wavelength double cones and in single short wavelength (S) cones, respectively. The light absorption of ellipsosomes indicated the presence of reduced cytochrome-c with the highest optical densities found in the M members of L/M double cones. By contrast, S cones contained pseudo-ellipsosomes which had very low optical density. UV cones were present everywhere as part of square or row mosaics in the retina of F. heteroclitus. Cone packing was on average higher for locations in the upper half of the retina while the highest cone density was found in the centro-ventral retina. An analysis of potential quantum catches for each cone type as a function of retinal sector and underwater irradiance characteristics revealed higher overall quantum catches for cones in the upper retina when the light field was assumed homogeneous, and higher quantum catches for cones in the lower retina when downwelling, horizontal, and upwelling irradiances were considered separately. At dusk, quantum catch was highest for M cones and the contribution to the overall retinal quantum catch by UV and S cones was much greater than during daylight hours. We propose that UV and S cones may be used to detect targets of interest against the background irradiance sensed by double cones.

We report on the temporal properties of the spontaneous bursts of activity in the developing turtle retina. Quantitative statistical criteria were used to detect, cluster, and analyze the temporal properties of the bursts. The interburst interval, duration, firing rate, and number of spikes per burst varied widely among cells and from burst to burst in a single cell. Part of this variability was due to the positive correlation between a burst's duration and the interburst interval preceding that burst. This correlation indicated the influence of a refractory period on the bursts' properties. Further evidence of such a refractoriness came from the bursts' auto-covariance function, which gives the tendency of a spike to occur a given amount of time after another spike. This function showed a positive phase (between ≈10 ms and 10 s) followed by a negative one (between 10 s and more than 100 s), suggestive of burst refractoriness. The bursts seemed to be propagating from cell to cell, because there was a long (symmetrically distributed) delay between the activation of two neighbor cells (median absolute delay = 2.3 s). However, the activity often failed to propagate from one cell to the other (median safety factor = 0.59). The number of spikes per burst in neighbor cells was statistically positively correlated, indicating that the activity in the two cells was driven by the same excitatory process. At least two factors contribute to the excitability during bursts, because the positive phase of the cross-covariance function (similar to auto-covariance but for two cells) had a temporally asymmetric fast component (1–3 ms) followed by a temporally symmetric slow component (1 ms to 10 s).

Acetylcholine (ACh) in the vertebrate retina affects the response properties of many ganglion cells, including those that display directional selectivity. Three β and eight α subunits of neuronal nicotinic acetylcholine receptors (nAChRs) have been purified and antibodies have been raised against many of them. Here we describe biochemical and immunocytochemical studies of nAChRs in the rabbit retina. Radioimmunoassay and Western blot analysis demonstrated that many of the nAChRs recognized by a monoclonal antibody (mAb210) contain β2 subunits, some of which are in combination with α3 and possibly other subunits. MAb210-immunoreactive cells in the inner nuclear layer (INL) were 7–14 μm in diameter and were restricted to the innermost one or two tiers of cells, although occasional cells were found in the middle of the INL. At least 60% of the cells in the ganglion cell layer (GCL) in the visual streak displayed mAb210 immunoreactivity; these neurons ranged from 7–18 μm in diameter. The dendrites of cells in both the INL and GCL could sometimes be followed until they entered one of two dense, poorly defined, bands of processes in the inner plexiform layer (IPL) that overlap the arbors of the cholinergic starburst cells. Parvalbumin and serotonin-positive neurons did not exhibit nAChR immunoreactivity. Although the level of receptor expression appeared to be low, mAb210 immunoreactivity was observed in some of the ChAT-positive (starburst) amacrine cells.

Lateral inhibition is one of the first and most important stages of visual processing. There are at least four theories related to information theory in the literature for the role of early retinal lateral inhibition. They are based on the spatial redundancy in natural images and the advantage of removing this redundancy from the visual code. Here, we contrast these theories with data from the retina's outer plexiform layer. The horizontal cells' lateral-inhibition extent displays a bell-shape behavior as function of background luminance, whereas all the theories show a fall as luminance increases. It is remarkable that different theories predict the same luminance behavior, explaining “half” of the biological data. We argue that the main reason is how these theories deal with photon-absorption noise. At dim light levels, for which this noise is relatively large, large receptive fields would increase the signal-to-noise ratio through averaging. Unfortunately, such an increase at low luminance levels may smooth out basic visual information of natural images. To explain the biological behavior, we describe an alternate hypothesis, which proposes that the role of early visual lateral inhibition is to deal with noise without missing relevant clues from the visual world, most prominently, the occlusion boundaries between objects.

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.

To further characterize the H1 and H2 horizontal cell populations in macaque monkey retinae, cells were injected with the tracer Neurobiotin following intracellular recordings. Tracer coupling between cells of the same type revealed all H1 or H2 cells in small patches around the injected cell. The mosaics of their cell bodies and the tiling of the retina with their dendrites were analyzed. Morphological differences between the H1 and H2 cells observable in Neurobiotin-labeled patches made it possible to recognize H1 and H2 cells in retinae immunolabeled for the calcium-binding proteins parvalbumin and calbindin, and thus to study their relative spatial densities across the retina. These data, together with the intracellularly stained patches, show that H1 cells outnumber H2 cells at all eccentricities. There is, however, a change in the relative proportions of H1 and H2 cells with eccentricity: close to the fovea the ratio of H1 to H2 cells is ∼4 to 1, in midperipheral retina ∼3 to 1, and in peripheral retina ∼2 to 1. In both the Neurobiotin-stained and the immunostained retinae, about 3–5% of the H2 cells were obviously misplaced into the ganglion cell layer. Several features of the morphology of the misplaced H2 cells suggest that they represent the so-called “biplexiform ganglion cells” previously described in Golgi studies of primate retina.

Ganglion cells responding only transiently to changes in illumination are found in many different vertebrate retinas. The interactions underlying formation of these transient responses are still poorly understood. Two recently proposed hypotheses are (1) functional inhibitory pathways are necessary for transient response production, and (2) direct inhibition of the ganglion cell has little effect on its output. Here, we examine these conclusions by using cell-attached patch-clamp recordings of spiking, whole-cell recordings of synaptic currents, and computer modeling. We found that picrotoxin (a GABAA and GABAC receptor antagonist), bicuculline (a GABAA receptor antagonist), and strychnine (a glycine receptor antagonist), applied either singly or in combination, always failed to convert transient responses to sustained responses. Application of the GABAB antagonist CGP35348 in the presence of picrotoxin and strychnine also failed to convert transient responses into sustained responses. Whole-cell recordings of synaptic currents at various holding potentials indicated that direct inhibitory inputs to ganglion cells limit the duration of net excitation, implying that direct inhibition does act to truncate the ganglion cell spiking response. Computer simulations using spiking and synaptic data from combined cell-attached and whole-cell recordings supported this interpretation. We conclude that inhibitory pathways are not required for generation of transient responses, but these pathways do serve to modulate transient ganglion cell spiking responses. We find that this modulation occurs, in part, via inhibitory inputs directly to the ganglion cell.

To date, two cannabinoid receptors, CB1 and CB2, have been cloned. The CB1 receptor has been found in a variety of tissues, particularly in the brain. CB2 receptor mRNA is mainly expressed in the immune system, though one group has found it in mouse cerebellum. Previous immunostaining studies in our lab demonstrated the presence of CB1 receptors in the retina though little evidence exists for the presence of CB2. The putative endogenous ligand for CB2 has been found in retina, however, suggesting that further study of CB2 in retina is warranted. Because glutamate is toxic to retinal ganglion cells in glaucoma and activation of CB2 receptors may be able to protect neurons from glutamate-induced death, we examined the expression of CB2 mRNA in adult rat retina in order to better understand possible neuroprotective mechanisms relevant to glaucoma. Using in situ hybridization, we demonstrated that CB2 cannabinoid receptor messenger RNA was clearly expressed in the adult rat retina, including the somas of retinal ganglion cells. Antisense cRNA probe detected strong signals in the retinal ganglion cell layer, the inner nuclear layer, and the inner segments of photoreceptor cells. Using reverse transcription polymerase chain reaction (RT-PCR) in both rat and mouse tissue, we obtained an RT-PCR product with the same sequence as that reported for CB2 in the GenBank database, thus confirming the presence of CB2 mRNA in retina. The presence of CB2 in retina provides new evidence for the presence of CB2 in the central nervous system (CNS) and an excellent model for its study.

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.

The avian retinotectofugal pathway has been suggested to be homologous to the mammalian retinotectofugal pathway. The projection of the nucleus rotundus upon the ectostriatum is equivalent to that of the pulvinar nucleus upon the extrastriate cortex in mammals. In this system, the optic tectum relays retinal input to the nucleus rotundus, which then ascends to the ectostriatum of the telencephalon. Given the fact that the chick retinotectofugal system becomes mature early during development, the present study attempted to investigate the timecourse of neuronal connections of the embryonic rotundoectostriatal pathway. We used multiple injections of cholera toxin B subunit (CTb) in the ectostriatum of chick embryos to retrogradely trace projections to the nucleus rotundus. We found CTb-labeled neurons in the nucleus rotundus at embryonic day 7.5–8. By embryonic day 8–8.5, increased numbers of CTb-labeled neurons were seen in the nucleus rotundus. It was noted that the time of this initial connection between the nucleus rotundus and the ectostriatum is nearly synchronous with that of the retinotectal and tectorotundal pathways, respectively (Crossland et al., 1975; Thanos & Bonhoeffer, 1987; Wu et al., 2000). These findings, combined with the present study, suggest that the retinotectofugal system becomes established, at least at a structural level, by embryonic day E8.

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.

Recently, it was reported that the polyunsaturated fatty acids (PUFAs), arachidonic acid (AA) and linolenic acid (LNA), activate the light-sensitive channels in Drosophila photoreceptors (Chyb et al. 1999). We have examined whether these PUFAs activate the light-sensitive channels in Limulus ventral photoreceptors. We find that, whether applied from the outside or injected into a Limulus ventral photoreceptor, either AA or LNA fails to activate the light-sensitive channels. Moreover, the synthetic diacylglycerol analog, 1-oleoyl-2-acetyl-sn-glycerol, also fails to activate the light-sensitive channels. We suggest that these findings require us to rethink our view about the generality of the process of phototransduction in invertebrate microvillar photoreceptors. We propose that the photoreceptors of Drosophila and Limulus evolved to utilize different branches of the phosphoinositide pathway for phototransduction: those of Limulus evolved to utilize IP3-mediated calcium release while those of Drosophila evolved to utilize diacylglycerol and it's downstream products.

In addition to the well-studied AII amacrine cell, there is another amacrine cell type participating in the rod pathway of the mammalian retina. In cat, this cell is called the A17 amacrine cell, and in rabbits, it is called the indoleamine-accumulating amacrine cell (S1 and S2); however, the presence of the corresponding cell type has not yet been described in detail for the rat retina. To this end, we injected amacrine cells with Neurobiotin in vertical retinal slices. After histological processing, we were able to reconstruct the morphology of a wide-field amacrine cell which showed characteristics of A17 and S1/S2 amacrine cells. The rat wide-field amacrine cells exhibited the same stratification pattern, their dendrites bore varicosities and ramified in sublamina 5 of the inner plexiform layer (IPL), and they were dye-coupled to other amacrine cells. To determine whether those amacrine cells shared electrophysiological characteristics as well, we performed whole-cell patch-clamp recordings and examined their voltage-activated currents and neurotransmitter-induced currents. We never observed voltage-gated Na+ currents and spike-like potentials upon depolarization by current injection in these cells. We identified GABA- and glycine-sensitive Cl− currents that could be blocked by bicuculline and strychnine, respectively. We also observed kainate- and AMPA-activated currents, which could be inhibited by the application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Finally, a 400-ms full-field light stimulus was used to characterize the light responses of A17 amacrine cells. The light ON-induced inward current could be suppressed by the application of 2,3-Dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulphonamide (NBQX), while the majority of the light OFF-induced current was inhibited by bicuculline and reduced to a smaller extent by NBQX. CPP, an NMDA blocker, had no effect on the light response of rat A17 amacrine cells.

The physiological and morphological properties of color-opponent bipolar cells in the carp retina were studied. Fifty nine OFF-center bipolar cells and 63 ON-center bipolar cells out of about 500 total bipolar cells recorded showed color-opponent responses. The OFF-center color-opponent bipolar cells were classified into three subgroups according to their spectral and spatial responses. Fifty OFF-center color-opponent cells responded with depolarization to a blue light spot and with hyperpolarization to a red spot in the receptive-field center. The polarity of the surround response was opposite to that of center response at each wavelength. Therefore these cells were classified as OFF double-opponent cells (OFF-DO). Eight cells responded with hyperpolarization to a blue and green spot and with depolarization to a red spot. The surround responses of those cells were depolarizing at any wavelength (R+G− cell). One responded with hyperpolarization to a blue and red spot and with depolarization to a green spot. The surround response showed a different spectral characteristic from that of the center response. It responded with depolarization to a blue and green annulus and with hyperpolarization to a red annulus (R−G+B− cell). The ON-center color-opponent bipolar cells were similarly classified into three subgroups. Sixty of ON-center color-opponent cells were the double color-opponent type (ON-DO cell), showing the responses of opposite polarity to the OFF-DO cells. Two cells were classified as R−G+ cell, and one cell as R+G−B+ cell. Both OFF- and ON-DO cells were identified by their morphology as Cajal's giant bipolar cells, and R+G−, R−G+, R−G+B−, and R+G−B+ cells as Cajal's small bipolar cells. The analysis of the latency and the ionic mechanisms of their responses suggest that DO cells under light-adapted conditions receive direct inputs from long-wavelength (red) cones, RG cells from middle-wavelength (green) cones, and RGB cells from short-wavelength (blue) cones. Possible mechanisms of the opponent inputs to these bipolar cells are discussed.

In the mature rabbit retina, two classes of horizontal cells, A type and B type, provide lateral inhibition in the outer plexiform layer (OPL) and spatially modify the activation of bipolar cells by photoreceptors. Gap junctions connecting homologous horizontal cells determine the extent to which this inhibitory activity spreads laterally across the OPL. Little is currently known about the expression of gap junctions in horizontal cells during postnatal development or how cell–cell coupling might contribute to subsequent maturational events. We have examined the morphological attributes and coupling properties of developing A and B type horizontal cells in neonatal rabbit retina using intracellular injections of Lucifer Yellow and Neurobiotin. Prelabeling with DAPI permitted the targeting of horizontal cell bodies for intracellular injection in perfused preparations of isolated retina. A and B type horizontal cells were identifiable at birth although their dendritic field sizes had not reached adult proportions and their synaptic contacts in the OPL were minimal. Both cell types exhibited homologous dye coupling at birth. Similar to that seen in the adult, no heterologous coupling was observed, and homologous coupling among A type cells was stronger than that observed among B type cells. The spread of tracer compounds through gap junctions of morphologically immature horizontal cells suggests that ions and other small, bioactive compounds may likewise spread through coupled, horizontal networks to coordinate the subsequent maturational of emerging outer plexiform layer pathways.

The inhibitory neurotransmitter gamma aminobutyric acid (GABA) has been shown to influence the responses of ganglion cells in the mammalian retina. Consistently, GABAA receptor subunits have been localized to different ganglion cell types. In this study, the distribution of the α1 subunit of the GABAA receptor on the dendrites of midget and parasol ganglion cells was investigated quantitatively in the retina of a New World monkey, the marmoset. Ganglion cells were injected with Neurobiotin in a live in vitro retinal whole-mount preparation. Retinal pieces were then processed with an antibody against the α1 subunit of the GABAA receptor. Strong punctate immunoreactivity indicative of synaptic localization is present in the ON and OFF sublamina of the inner plexiform layer. Many of the immunoreactive puncta coincide with the dendrites of both midget and parasol ganglion cells. Immunoreactive puncta are present on distal and proximal dendrites of ON and OFF cells of both ganglion cell types. On average, parasol cells show a slight increase in the spatial density of immunoreactive puncta with distance from the soma, whereas the density of immunoreactive puncta on midget cells stays even. Parasol ganglion cells show a slightly higher average density of immunoreactive puncta (0.083 puncta/μm dendrite) than midget cells (0.054 puncta/μm dendrite).