Neurons likely to utilize glycine (GLY) as a neurotransmitter were identified immunocytochemically in the “all-cone” lizard retina and the basic anatomical organization of the retinal GLY and gamma-aminobutyric acid (GABA) systems was compared. Four types of GLY-immunoreactive (GLY-IR) neurons were identified. Most GLY-IR cells were amacrine cells, which comprised at least two types. GLY-IR interplexiform cells and ganglion cells also were identified. The first GLY-IR amacrine cell type was characterized by a small pyriform soma, located distal to the border of the inner plexiform layer (IPL), and fine dendrites. Most GLY-IR amacrine cells were of this type and several subtypes may exist within this group. The second amacrine cell type was characterized by a large, distally located soma and a large descending process. This amacrine cell type showed colocalization of GLY-IR and GABA-IR and comprised about 4% of the total GLY-IR amacrine cell population.

Comparison of GLY-IR and GABA-IR on serial sections showed that GLY and GABA were present in largely separate neuronal populations. Generally, GLY-IR amacrine cells were smaller, more distally located in the inner nuclear layer and had finer dendrites than GABA-IR amacrine cells. Distribution of GLY-IR and GABA-IR in the outer plexiform layer and the inner plexiform layer differed considerably.

Based on the segregated distribution of GLY-IR and GABA-IR in the synaptic layers of the lizard retina, GLY and GABA may have fundamentally different roles in retinal processing.

Lateral suprasylvian visual cortex in the cat has been studied extensively, but its retinotopic organization remains controversial. Although some investigators have divided this region into many distinct areas, others have argued for a simpler organization. A clear understanding of the region’s retinotopic organization is important in order to define distinct areas that are likely to subserve unique visual functions. We therefore reexamined the map of the lower visual field in the striate-recipient region of lateral suprasylvian cortex, a region we refer to as the lateral suprasylvian area, LS.

A dual mapping approach was used. First, receptive fields were plotted at numerous locations along closely spaced electrode penetrations; second, different anterograde tracers were injected at retinotopically identified sites in area 17, yielding patches of label in LS. To visualize the resulting data, suprasylvian cortex was flattened with the aid of a computer.

Global features of the map reported in many earlier studies were confirmed. Central visual field was represented posteriorly, and elevations generally shifted downward as one moved anteriorly. Often (though not always) there was a progression from peripheral locations towards the vertical meridian as the electrode moved down the medial suprasylvian bank.

The map had some remarkable characteristics not previously reported in any map in the cat. The vertical meridian’s representation was split into two pieces, separated by a gap, and both pieces were partially internalized within the map. Horizontal meridian occupied the gap. The area centralis usually had a dual representation along the posterior boundary of the lower field representation, and other fragments of visual field were duplicated as well. Finally, magnification appeared to change abruptly and unexpectedly, so that compressed regions of representation adjoined expanded regions. Despite its complexity, we found the map to be more orderly than previously thought. There was no clearcut retinotopic basis on which to subdivide LS’s lower field representation into distinct areas.

We have investigated the distribution of ON- and OFF-center responses in the lateral geniculate nucleus of ferrets with normal and abnormal retinal projections. Electrophysiological recordings in normal pigmented animals confirm previous studies on mustelids showing that ON-center responses are found in the anterior, inner parts of laminae A and AI and OFF-center responses in posterior, outer leaflets. In albino animals, lamina A displays normal patterns of ON/OFF segregation but in lamina AI, which receives an abnormal crossed retinal projection, no consistent patterns of segregation are found. Following monocular enucleation on the day of birth, the uncrossed projection in pigmented ferrets remains expanded across the LGN. Anatomically and physiologically, this projection is segregated into two leaflets: an anterior, inner ON-center leaflet and a posterior outer OFF-center leaflet. We conclude that the persistence of ON/OFF segregation, independent of geniculate location, suggests that self-sorting of retinal input is an important factor in generating the segregation.

Although inositol trisphosphate (InsP3) is a key substance in phototransduction of invertebrate photoreceptors, its intracellular concentration remains unknown. The purpose of this study was to assay its concentration and the concentration of its precursor, phosphatidylinositol bisphosphate (PtdInsP2), within squid photoreceptors. Rhabdomeric membranes were purified and their PtdInsP2 content measured with a phosphate assay after the extracted phospholipids were deacylated and separated by ion-exchange chromatography. At least 75% of the total PtdInsP2 found in the retinal homogenate was associated with the plasma membranes of the rhabdomeric microvilli, where PtdInsP2 was 3.1 ± 0.7% of the total phospholipids, a level comparable to values published for rat brain. In terms of rhodopsin, microvillar membranes contained 3.7 ± 0.9 mol PtdInsP2/mol rho. The InsP3 content of living retinas was measured with a radioreceptor assay. The basal content of dark-adapted retinas was 0.15 ± 0.05 InsP3/rho, equivalent to 30 ± 9 nmol/g tissue that is about twice that of rat brains. Flash illumination (≈lms in duration) that photoactivated 1% of rhodopsin increased the level about fivefold to 0.68 ± 0.22 lnsP3/rho. Corresponding decrease in PtdInsP2 was undetectable as it was within measurement errors. For PtdInsP2, the measured content corresponds to 5.6 ± 1.4 mM within the volume of rhabdomere. Maximal light-induced concentration of InsP3 is calculated to be 1.2 ± 0.4 mM within the cytoplasm of the distal segment. Each photoactivated rhodopsin leads to the formation of 500 InsP3 molecules when measured 15 s after the flash. Thus, high concentration of InsP3 in these cells is primarily due to restricted intracellular volumes rather than to high amplification by the enzyme cascade. The InsP3 concentration within squid photoreceptors is the highest yet reported for any transducing cell and may indicate the involvement of relatively low affinity receptors or channels during invertebrate phototransduction.

In a dichromatic teleost species, we determined the intensity of light of various wavelengths required to prevent cone elongation by exposing fish at the time of their normal “dusk” phase to monochromatic light (479, 623, and 660 nm) at eight to ten different intensities for 75 min. The positions of single and double cones were measured in tangential sections and expressed as cone indices. At all wavelengths, the spectral responses of both cone types were virtually identical. Furthermore, the sensitivity of the blocking effect was highest at shorter wavelengths. When comparing the relative quantal sensitivities of myoid elongation for the two cone types to the spectral sensitivities of the three types of Aequidens pulcher photoreceptor, we found the closest match between the action spectrum and the absorption spectrum of the green-sensitive single cones. This may indicate that this cone type is capable of reacting directly to decreasing levels of illumination. On the other hand, the identical sensitivity of both cone types argues for an indirect control mechanism of dark-adaptive cone elongation, possibly via a neural pathway involving the inner retinal layers, complementary to the neural control of light adaptation. Green-sensitive single cones are well suited to trigger this response, since (1) their sensitivity is inferior to that of double cones; (2) waters inhabited by the blue acara transmit best at long wavelengths; and (3) at dusk, long-wavelength radiation dominates over other parts of the spectrum. Therefore, green-sensitive cone threshold will be reached first at dusk.

Two basic types of cholinergic receptor have been identified in nervous systems: nicotinic and muscarinic. In the mammalian visual system, the balance of evidence suggests that nicotinic activity is associated primarily with transmission and processing of information while muscarinic activity reflects modulatory influences arising in the brainstem and basal forebrain. We have measured contrast sensitivity functions using a two-alternative forced-choice procedure in young human volunteers with and without administration of nicotine (1.5 mg by buccal absorption) or the muscarinic antagonist scopolamine (1.2 mg orally). Scopolamine elevates contrast-detection thresholds uniformly at all spatial frequencies, consistent with blocking of a nonspecific arousal system. Nicotine, in contrast, improves sensitivity at low spatial frequencies (below about 4 cycle/deg); at higher spatial frequencies sensitivity is, if anything, impaired. Using counterphase gratings, we find that scopolamine elevates thresholds uniformly at all temporal frequencies. Nicotine lowers thresholds at high but not low temporal frequencies. The results obtained with nicotine suggest that contrast sensitivity reflects the activity of two mechanisms, or sets of spatiotemporal filters, that are pharmacologically distinct, the contrast sensitivity function reflecting the envelope of their sensitivities.

Previous research suggests that plaid-induced motion aftereffects (MAEs) involve extrastriate mechanisms (Wenderoth et al., 1988). There is evidence also that binocular rivalry occurs beyond VI and that it disrupts the processing of MAEs which are believed to be based upon extrastriate mechanisms (e.g. the spiral MAE) but not MAEs, such as linear MAE induced by a drifting grating, which are thought to arise in striate cortex (Wiesenfelder & Blake, 1990). The logical inference is that binocular rivalry during drifting plaid-induced adaptation should reduce the MAEs which result. We report experiments which confirm this prediction.

In previous electrophysiological experiments from hypopigmented animals (mice, rats, rabbits), single-unit recordings from both retinal ganglion axons and cells in the superior colliculus have demonstrated an increase in threshold in the dark-adapted state which is roughly proportional to the animal's ocular melanin concentration. We have examined the thresholds in hypopigmented mice by using a behavioral water maze screening test and found similar threshold elevations to the electrophysiology. In the present study, we investigated the contribution of retinal light damage to the threshold elevation in an albino mouse strain which is relatively resistant to light damage (C57BL/6J c2J/c2J) and mice with profound retinal degeneration (C57BL/6J rd/rd).

Black or albino littermates (C57BL/6J + / c2J or c2J / c2J) were placed in either constant light (350 cd/m2) or dim cycling light (0.001 cd/m2) for 21 days before testing. The normally pigmented animals had thresholds of 1.00 × 10−5 cd/m2 regardless of their light history. The albino mice (c2J/c2J) maintained in constant light had a slight 0.30 log unit elevation compared to their controls that were maintained in dim cycling light 6.3 × 10−4 cd/m2 (similar to previously published reports).

We examined the retinal morphology of representative animals in semi-thin plastic sections. We could not detect any light damage (overall morphology or cell counts in the outer-nuclear layer) in either the normally pigmented animals or the albino mice (c2J/c2J) maintained in dim cycling light. We found extensive light damage in the albino mice (c2J/c2J) maintained in constant light (virtual absence of photoreceptor outersegments) that corresponded to the slight elevation in threshold. We conclude that the elevation in threshold found in albino mice (c2J/c2J) maintained in dim cycling light is not the result of light damage. These results support our previous findings that the sensitivity defect in hypopigmented animals is proportional to the degree of ocular hypopigmentation.

In in-vitro preparations of both macaque and human retina, intracellular injections of Neurobiotin and horseradish peroxidase were used to characterize the morphology, depth of stratification, and mosaic organization of a type of bistratified ganglion cell. This cell type, here called the small bistratified cell, has been shown to project to the parvocellular layers of the dorsal lateral geniculate nucleus (Rodieck, 1991) and is therefore likely to show color-opponent response properties.

In both human and macaque, the two dendritic tiers of the bistratified cell are narrowly stratified close to the inner and outer borders of the inner plexiform layer. The inner tier is larger in diameter and more densely branched than the outer tier and gives rise to distinct spine-like branchlets bearing large, often lobulated heads. By contrast the smaller, outer tier is sparsely branched and relatively spine-free.

In human retina, the small bistratified cells range in dendritic field diameter from ∼50 µm in central retina to ∼400 µm in the far periphery. The human small bistratified cells are about 20% larger in dendritic-field diameter than their counterparts in the macaque. However, when the difference in retinal magnification between human and macaque is taken into account, the small bistratified cells are similar in size in both species. In macaque, the small bistratified cell has a dendritic-field size that is ~10% larger than that of the magnocellular-projecting parasol ganglion cell. Human small bistratified ganglion cells tend to have smaller dendritic-field diameters than parasol cells. This is because parasol ganglion cells are larger in human than in macaque retina (Dacey & Petersen, 1992).

In macaque retina, intracellular injections of Neurobiotin revealed heterotypic tracer coupling to a distinct mosaic of amacrine cells and probable homotypic coupling to an array of neighboring ganglion cells around the perimeter of the injected cell's dendritic tree. The amacrine cell mosaic had a density of 1700 cells/mm2 in peripheral retina. Individual amacrines had small, densely branched and bistratified dendritic fields. From the homotypic coupling, it was possible to estimate for the small bistratified cell a coverage factor of ~1.8, and a density of ~1% of the total ganglion cells in central retina, increasing to ~6–10% in the retinal periphery.

The estimated density, dendritic-field size, and depth of stratification all suggest that the small bistratified ganglion cell type is the morphological counterpart of the common short-wavelength sensitive or ‘blue-ON’ physiological type.

Dendrites of retinal ganglion cells (RGCs) tend to be distributed preferentially toward areas of reduced RGC density. This, however, does not occur in the retina of normal pigmented rats, in which it has been suggested that the centro-peripheral gradient of RGC density is too shallow to provide directional guidance to growing dendrites. In this study, laterally displaced dendrites of RGCs retrogradely labeled with horseradish peroxidase were related to cell density gradients induced experimentally in the rat retina. Neonatal unilateral lesions of the optic tract produced retrograde degeneration of contralaterally projecting RGCs, but spared ipsilaterally projecting neurons in the same retina. These lesions created an anomalous temporal to nasal gradient of cell density across the decussation line, opposite to the nasal to temporal gradient found along the same axis in either normal rats or rats that had the contralateral eye removed at birth. RGCs in rats that received optic tract lesions had their dendrites displaced laterally toward the depleted nasal retina, while in either normal or enucleated rats there was no naso-temporal asymmetry. The lateral displacement affected both primary dendrites and higher-order branches. However, the gradient of cell density after optic tract lesions was less steep than the gradient in either normal or enucleated rats. To test for the presence of steeper gradients at early stages of development, RGC density gradients were also examined at postnatal day 5 (P5). In normal rats, the RGCs were homogeneously distributed throughout the retina, while rats given optic tract lesions at birth already showed a temporo-nasal density gradient at P5. Still, this anomalous gradient was less steep than that found in normal adults. It is concluded that the time course, rather than the steepness of the RGC density gradient, is the major determinant of the lateral displacement of dendritic arbors with respect to the soma in developing RGCs. The data are consistent with the idea that the overall shape of dendritic arbors depends in part on dendritic competition during retinal development.

The role of dopamine as the endogenous signal-initiating light-dependent changes in the distribution of pigment granules in goldfish retinal pigment epithelium was investigated. In normal retinas, light adaptation resulted in the dispersion of pigment granules. This effect of light was mimicked by the intraocular injection of dopamine or serotonin, which is thought to increase endogenous dopamine release, into dark-adapted eyes. The effect of light, dopamine, or serotonin on dark-adapted retinas was blocked by the dopamine receptor antagonists haloperidol and sulpiride. However, lesioning the endogenous source of retinal dopamine, by prior intraocular injection of 6-hydroxydopamine (6-OHDA), did not block the dispersion of pigment granules in light-adapted retinas. No significant differences in pigment dispersion were noted between unlesioned and lesioned light- or dark-adapted retinas. However, the effect of light on pigment dispersion was no longer blocked by haloperidol or sulpiride in 6-OHDA lesioned animals. Dopamine and serotonin mimicked the effect of light when injected into lesioned dark-adapted eyes, but their effects were also not blocked by haloperidol or sulpiride. These results suggest that dopamine, acting on D2 receptors, is sufficient to induce pigment migration in unlesioned animals. In 6-OHDA-lesioned animals, however, pigment migration is mediated by a receptor mechanism other than D2.

The classically defined receptive fields of V4 cells are confined almost entirely to the contralateral visual field. However, these receptive fields are often surrounded by large, silent suppressive regions, and stimulating the surrounds can cause a complete suppression of response to a simultaneously presented stimulus within the receptive field. We investigated whether the suppressive surrounds might extend across the midline into the ipsilateral visual field and, if so, whether the surrounds were dependent on the corpus callosum, which has a widespread distribution in V4. We found that the surrounds of more than half of the cells tested in the central visual field representation of V4 crossed into the ipsilateral visual field, with some extending up to at least 16 deg from the vertical meridian. Much of this suppression from the ipsilateral field was mediated by the corpus callosum, as section of the callosum dramatically reduced both the strength and extent of the surrounds. There remained, however, some residual suppression that was not further reduced by addition of an anterior commissure lesion. Because the residual ipsilateral suppression was similar in magnitude and extent to that found following section of the optic tract contralateral to the V4 recording, we concluded that it was retinal in origin. Using the same techniques employed in V4, we also mapped the ipsilateral extent of surrounds in the foveal representation of VI in an intact monkey. Results were very similar to those in V4 following commissural or contralateral tract sections. The findings suggest that V4 is a central site for long-range interactions both within and across the two visual hemifields. Taken with previous work, the results are consistent with the notion that the large suppressive surrounds of V4 neurons contribute to the neural mechanisms of color constancy and figure-ground separation.

Electroretinogram (ERG) flicker photometry was used to examine the photopigment complements of representatives of four genera of Canid: domestic dog (Canis familiaris), Island gray fox (Urocyon littoralis), red fox (Vulpes vulpes), and Arctic fox (Alopex lagopus). These four genera share a common cone pigment complement; each has one cone pigment with peak sensitivity of about 555 nm and a second cone pigment with peak at 430–435 nm. These pigment measurements accord well with the conclusions of an earlier investigation of color vision in the dog, and this fact allows some predictions about color vision in the wild canids. An additional set of measurements place the peak of the dog rod pigment at about 508 nm.

The performance of pigeons on a color-reversal learning task was assessed after thalamic lesions disrupting the thalamofugal and tectofugal visual pathways. Successful performance of a simultaneous color discrimination was accomplished after surgery, and a series of reversals of the original discrimination followed during which the positive and negative consequences associated with the stimuli were interchanged. Shimizu and Hodos (1989) had reported that lesions of two laminae in the visual wulst (IHA and HD), both targets of the avian thalamofugal pathway, resulted in increased errors in a color-reversal learning task in pigeons. This finding suggested that the thalamofugal pathway might play a role in visual discrimination involving stimulus context changes. In the present study, lesions of the OPT complex (the thalamic source of afferents to IHA and HD) were found to have no effect on color-reversal learning performance. Instead, we found that damage to nucleus rotundus (the thalamic component of the tectofugal pathway) resulted in deficits that were far in excess of those that had been obtained after IHA and HD lesions. We suggest that the color-reversal learning deficits after Wulst lesions are not due to the Wulst's connections with the thalamofugal pathway, but rather to its connections with the tectofugal pathway.

Interocular alignment was assessed by corneal light reflex photography in 15 normal and 26 strabismic kittens. Strabismus was induced at 3–4 weeks of age by severing one extraocular muscle (tenotomy), by cutting and reinserting the muscle at another position on the ocular globe (recession), or by combining recession of the medial rectus muscle with resection of the lateral rectus muscle of the same eye. Nineteen strabismic and five normal kittens were followed longitudinally from 12 days to about 6 months of age.

Three out of the six longitudinally followed tenotomized cats and six out of the 13 recessed cats conserved their postoperative ocular deviation throughout the testing period (“large-angle strabismics”). Three tenotomized and seven recessed cats showed a transient deviation for 1–2 weeks after surgery, after which the interocular deviation diminished to values found in normal cats (“microstrabismic” cats). Both recessed-resected cats showed a transient interocular deviation.

In spite of their different developmental histories, all cats showed a clear breakdown of binocularity in area 17. Large-angle strabismics showed a dominance of the non-operated eye, while in microstrabismic cats, both eyes were equally effective in driving cortical cells. It thus appears that a transient strabismus is sufficient to produce a reduction of binocularity in area 17.

We present microspectrophotometric evidence for the existence of two distinct visual pigments residing in two different morphological types of photoreceptor of the sea lamprey. In the upstream migrant Petromyzon marinus, the pigment found in short receptors has a wavelength of peak absorbance (λmax) of 525 nm, whereas the pigment located in long receptors has a λmax of 600 nm. Although the former appears to be pure porphyropsin, the latter is akin to visual pigments found in the red-absorbing cones of amphibian and teleost retinae. The kinship is more than superficial pertaining to λmax of the a–band absorbance to its native maximum value. The presence of an anion-sensitive and an anion-insensitive pigment in a retina implies the expression of two distinct opsin genes. We infer this from several examples of correlation between anion sensitivity and opsin sequence groupings. Moreover, the presence of two distinct opsin genes expressed throughout six vertebrate classes implies their existence in a common ancestor to all.

This study examined the influence of the pontomesencephalic peribrachial region (PBR) on the visual response properties of cells in the dorsal lateral geniculate nucleus (LGN). The response of single cells to a stationary flashing light spot was recorded with accompanying electrical stimulation of the PBR. The major objectives were to compare the effects of PBR stimulation on lagged and nonlagged cells, to examine how the visual response pattern of lagged cells could be modified by PBR stimulation and to examine whether the physiological criteria used to classify lagged and nonlagged cells are applicable during increased PBR input to the LGN. During PBR stimulation, the visual response was enhanced to a similar degree for lagged and nonlagged cells and the latency to half-rise of the visual response was reduced, particularly for the lagged X cells. The latency to half-fall of the visual response of lagged cells was not changed by PBR stimulation. Accordingly, the division of LGN cells into lagged and nonlagged cells based on visual response latencies was maintained during PBR stimulation. The initial suppression that a visual stimulus evokes in lagged cells was resistant to the effects of PBR stimulation. For the lagged cells, the largest response increase occurred for the initial part of the visual response. For the nonlagged cells, the largest increase occurred for the tonic part of the response. The results support the hypothesis that the differences in temporal response properties between lagged and nonlagged cells belong to the basic distinctions between these cell classes.

We measured transient and steady-state checkerboard contrast-reversal visual evoked potentials (VEPs) in ten dyslexics, five patient controls, and 11 normals over a range of contrasts and luminances. Latency, amplitude, and phase measurements failed to distinguish the responses of dyslexics from those of normals or patient controls. Decreases in luminance or contrast resulted in an increased latency of the transient VEP in all groups, but these changes also did not distinguish the responses of dyslexics from those of the controls. Response variability was similar in dyslexics and normals, but was increased in subjects with attention deficit-hyperactivity disorder (ADHD). Performance on standardized psychometric testing did differentiate the dyslexics from controls, but did not correlate with VEP responses.

The compartmental organization of visual cortical neurons was examined across species of primates by directly comparing the pattern of immunoreactivity for the 28-kD vitamin D-dependent calcium-binding protein (calbindin) in area 17 of squirrel monkeys, macaques, and neurologically normal adult humans. Area 17 of macaques and squirrel monkeys was similar in that somata and processes intensely immunoreactive for calbindin were present in the same layers (II-III, IVB, and V) and in both species formed a well-stained matrix that surrounded the CO-rich puffs in layer III. These intensely calbindin-immunoreactive neurons were identified as subpopulations of GABA-immunoreactive neurons. Among the most obvious differences in the two monkey species was the distribution of calbindin-positive elements outside of layer III: a dense immunostained matrix surrounded the puffs in layers II, IVB, V, and VI of squirrel monkeys but the immunostained neurons adopted no regular pattern outside layer III in macaques. In addition, although somata lightly immunoreactive for calbindin were present in both species, they were much more abundant in squirrel monkeys than macaques. The pattern of calbindin immunostaining in human area 17 resembled that of macaques in forming an intense matrix that surrounded puffs only in layer III, yet also resembled that of squirrel monkeys by including large numbers of lightly immunoreactive somata. These lightly immunostained somata included a very dense population forming a prominent band in layer IVA of human visual cortex. We conclude that for layer III of primary visual cortex, a similar pattern of neuronal chemistry exists across species of primates which is related to this layer's compartmental organization. Yet for other layers, the expression of calbindin immunoreactivity varies from one species to the next, perhaps reflecting variations in other neuronal properties.

Monoclonal antibodies to the three isozymes of protein kinase C (PKC) (α, β, and γ) were applied to postmortem human retina. Immunostaining was done on wholemount, or cryostat-sectioned retina, and visualized after ABC/DAB procedures by light (LM) and electron (EM) microscopy.

The PCK-α antibody stained rod bipolar cells throughout the retina. EM analysis confirmed they were PKC-α-immunoreactive (IR) on their characteristic dendritic and axonal synaptology. Putative blue cone bipolar cells with wide-field axon terminals, stratifying in s5 of the inner plexiform layer (IPL), were also PKC-α-IR, and EM showed them to engage in narrow-cleft ribbon junctions in blue cone pedicles.

The PKC-β antibody stained cone bipolar cells, many amacrine cells, and most ganglion cells. Cone bipolar cells were stained all the way into the foveal center: both midget and diffuse varieties were included. The IPL was densely PKC-IR and individual neurons could not be identified on stratification patterns. EM of the outer plexiform layer (OPL) revealed that both flat and invaginating cone bipolar types were IR and that IR axon terminals were presynaptic in all strata of the IPL. The occurrence of PKC-β-IR bipolar axons in stratum 2 of the IPL suggests that OFF-center as well as ON-center types were included.

The PKC-γ antibody gave inferior staining compared with results from the other two antibodies; however, two varieties of wide-field monostratified amacrine cell and a large-bodied ganglion cell type were discernible.

PKC in one form or another appears to be a second messenger used in neurotransmission by both rod and cone systems and ON- and OFF-center systems in the human retina.