The cholinergic amacrine cells of the rabbit retina form two mosaics placed symmetrically on either side of the inner plexiform layer. Recently, these cells have been reported to contain immunocytochemical markers for GABA. In this paper, we labeled the cholinergic cells with DAPI, then incubated the retina in [3H]-muscimol, a neuronal marker for GABA. Subsequently, we converted the DAPI fluorescence of the displaced cholinergic matrix to an opaque product by photooxidation in the presence of DAB. Autoradiography showed that all of the displaced cholinergic amacrine cells were labeled with ]3H]-muscimol, thus confirming the immunocytochemical results. The cholinergic cells account for approximately 80% of the cells in the ganglion cell layer which take up ]3H]-muscimol.

In the turtle retina the peptides met-enkephalin (metENK), somatostatin (SS), neurotensin (NT), and the indoleamine serotonin (5-HT) modulate ganglion cell (GC) activity. The predominant action of the peptides is excitatory, generally enhancing spontaneous firing and light-evoked activity. In contrast, 5-HT usually inhibits these GC activities. MetENK has both direct synaptic input onto GC and indirect action possibly via a GABA inhibitory interneuron. The metENK actions appear mediated via a mu-opiate receptor; morphine and D-ala-metENK-amide (DALA), a stable analog of metENK, are agonists. Naloxone antagonizes the actions of metENK and its agonists. DALA occasionally inhibits GC. This inhibition is antagonized by picrotoxin, while concurrent excitatory action on GC is enhanced. DALA enhances GC response at high spatial frequencies; naloxone attenuates it. The enhancement by DALA suggests a narrowed receptive-field (RF) center, possibly due to changes in a GABA-mediated inhibitory surround. 5-HT inhibitory actions are also mediated via direct and indirect synaptic pathways. 5-methoxy-dimethyl-tryptamine and methoxy-phenyl-piperazine are agonists of 5-HT action. They are both specific 5-HT1 agonists. LSD (lysergic acid diethylamide) and cyproheptadine, which act on 5-HT2 receptors, antagonize 5-HT actions in this retina. Strychnine enhances GC activity, probably by antagonizing glycine-mediated inhibitory inputs. It does not block the inhibitory action of 5-HT, which suggests that the indirect 5-HT inhibition is not mediated via a glycinergic interneurone. 5-HT suppresses directional selectivity (DS) and attenuates high spatial frequencies in some GC. This may be mediated via inhibition of GABAergic amacrines subserving DS and the RF inhibitory surround.

The distribution and ultrastructure of neurons and neuropil labeled by an antiserum to gamma-aminobutyric acid (GABA) were examined in the lateral geniculate nucleus (LGN) of the tree shrew (Tupaia belangeri). The LGN of this species segregates center type and cell class into three distinct pairs of laminae: a medial pair (laminae 1 and 2) containing ON-center cells, a more lateral pair (4, 5) containing OFF-center cells, and 2 laminae (3, 6) containing W-like cells. The relationship between this laminar segregation and the distribution of GABA immunoreactivity was investigated in the present study. GABA-immunoreactive neurons and neuropil were present in all six of the laminae. However, both the density of labeled cells (adjusted for neuronal density across laminae) and the density of labeled neuropil showed a medial-to-lateral gradient. The adjusted density of labeled cells was higher laterally than medially, and the density of labeled neuropil was significantly greater in the more lateral OFF-center laminae and W-like laminae than in the medial two ON-center laminae. Thus, inhibitory, GABAergic influences may modulate to different degrees the visual signals in the ON, OFF, and W pathways. Labeled cells had a mean cross-sectional area (107 μm2) approximately one-half that of unlabeled cells (216 μm2). They constitute 16–34% of the neurons in the LGN. At the electron microscope level, three different kinds of labeled profile were observed. Vesicle containing profiles like the F2 profiles of cat were postsynaptic to retinal terminals and presynaptic to conventional dendrites. Fl axon terminals with dense clusters of vesicles were also labeled as were some myelinated axons. Another labeled profile, which we suggest should be called an F3 process, was a large dendrite of irregular caliber with punctate groups of vesicles near the synapse. Our results suggest that GABAergic circuitry is an important part of the functional organization in the LGN of the tree shrew.

A geographical review of the published literature confirmed that red–green color-vision deficiency (Daltonism) is rare near the equator and more prevalent at higher latitudes, as others have reported. A survey of dictionaries of the languages spoken by the populations for which Daltonism data are available confirmed that distinct words for “blue” are also rare near the equator, and more common at higher latitudes. These results were compared to show an even stronger relation between the proportion of languages with a word for “blue” and the prevalence of Daltonism. We believe that the strong correlation between “blue” and Daltonism suggests that an evolutionary, physiological cause for both phenomena.

Retinal ganglion cells receive excitatory synapses from bipolar cells and inhibitory synapses from amacrine cells. Previous studies in primate suggest that the strength of inhibitory amacrine input is greater to cells in peripheral retina than to foveal (central) cells. A comprehensive study of a large number of ganglion cells at different eccentricities, however, is still lacking. Here, we compared the amacrine and bipolar input to midget and parasol ganglion cells in central and peripheral retina of marmosets (Callithrix jacchus). Ganglion cells were labeled by retrograde filling from the lateral geniculate nucleus or by intracellular injection. Presumed amacrine input was identified with antibodies against gephyrin; presumed bipolar input was identified with antibodies against the GluR4 subunit of the AMPA receptor. In vertical sections, about 40% of gephyrin immunoreactive (IR) puncta were colocalized with GABAA receptor subunits, whereas immunoreactivity for gephyrin and GluR4 was found at distinct sets of puncta. The density of gephyrin IR puncta associated with ganglion cell dendrites was comparable for midget and parasol cells at all eccentricities studied (up to 2 mm or about 16 degrees of visual angle for midget cells and up to 10 mm or >80 degrees of visual angle for parasol cells). In central retina, the densities of gephyrin IR and GluR4 IR puncta associated with the dendrites of midget and parasol cells are comparable, but the average density of GluR4 IR puncta decreased slightly in peripheral parasol cells. These anatomical results indicate that the ratio of amacrine to bipolar input does not account for the distinct functional properties of parasol and midget cells or for functional differences between cells of the same type in central and peripheral retina.

We studied how intrinsic membrane properties affect the gain and temporal pattern of response in bipolar cells dissociated from retinae of tiger salamanders. Currents specified by a pseudorandom binary sequence, an m-sequence, superimposed on various means, were injected into the cells. From the resultant membrane voltage response for each mean current, impulse responses were estimated. From each impulse response, transfer function, gain, and time constant were calculated. The bipolar cells acted as quasilinear adaptive filters whose gain and response speed are determined by the mean input current. Near resting potential, gain, and time constant were maximum. Dynamics were slow and low-pass, characterized by an approximately exponential impulse response. With depolarization, gains were reduced sharply, responses were much faster, and dynamics became band-pass, as indicated by an undershoot in the impulse response. For any given mean current, the shape of the impulse response did not depend on the amplitude of the m-sequence currents. Thus, bipolar cells behaved in a quasilinear fashion. The adaptive behavior was eliminated by blocking a potassium current, which implicates the role of a voltage-gated potassium conductance. Computer simulations on a model neuron including a delayed-rectifier reconstructed the observed behavior, and provided insight into other, less readily observable, parameters. Thus, bipolar cells, even when isolated, possess mechanisms which regulate, with unsuspected elaborateness, the sensitivities and dynamics of their responsiveness. Implications for adaptation and neuronal processing are discussed.

Acetylcholine is present in and released from starburst amacrine cells in the inner plexiform layer (IPL), but its role in retinal function except, perhaps, in early development, is unclear. Nicotinic acetylcholine receptors are thought to be present on ganglion, amacrine, and bipolar cell processes in the IPL, and it is known that acetylcholine increases the spontaneous and light-evoked responses of retinal ganglion cells. The effects of acetylcholine on bipolar cells are not known, and here we report the effects of nicotine on the b-wave of the electroretinogram in larval zebrafish. The b-wave originates mainly from ON-bipolar cells, and the larval zebrafish retina is cone-dominated. Only small rod responses can be elicited with dim lights in wild-type larval zebrafish retinas, but rod responses can be recorded over a range of intensities in a mutant (no optokinetic response f) fish that has no cone function. We find that nicotine strongly enhances cone-driven b-wave response amplitudes but depresses rod driven b-wave response amplitudes without, however, affecting rod- or cone-driven b-wave light sensitivity.

Specific variants of human long-wavelength (L) and middle-wavelength (M) cone opsin genes have recently been associated with a variety of vision disorders caused by cone malfunction, including red-green color vision deficiency, blue cone monochromacy, myopia, and cone dystrophy. Strikingly, unlike disease-causing mutations in rhodopsin, most of the cone opsin alleles that are associated with vision disorders do not have deleterious point mutations. Instead, specific combinations of normal polymorphisms that arose by genetic recombination between the genes encoding L and M opsins appear to cause disease. Knockout/knock-in mice promise to make it possible to study how these deleterious cone opsin variants affect the structure, function, and viability of the cone photoreceptors. Ideally, we would like to evaluate different variants that cause vision disorders in humans against a control pigment that is not associated with vision disorders, and each variant should be expressed as the sole photopigment in each mouse cone, as is the case in humans. To evaluate the feasibility of this approach, we created a line of mice to serve as the control in the analysis of disease-causing mutations by replacing exon 2 through 6 of the mouse M-opsin gene with the corresponding cDNA for a human L-opsin variant that is associated with normal vision. Experiments reported here establish that the resulting pigment, which differs from the endogenous mouse M opsin at 35 amino acid positions, functions normally in mouse cones. This pigment was evaluated in mice with and without coexpression of the mouse short wavelength (S) opsin. Here, the creation and validation of two lines of genetically engineered mice that can be used to study disease-causing variants of human L/M-opsins, in vivo, are described.

Opsins, like many other G-protein-coupled receptors, sustain constitutive activity in the absence of ligand. In partially bleached rods and cones, opsin's activity closes cGMP-gated channels and produces a state of “pigment adaptation” with reduced sensitivity to light and accelerated flash response kinetics. The truncated retinal analogue, β-ionone, further desensitizes partially bleached green-sensitive salamander rods, but enables partially bleached red-sensitive cones to recover dark-adapted physiology. Structural differences between rod and cone opsins were proposed to explain the effect. Rods and cones, however, also contain different transducins, raising the possibility that G-protein type determines the photoreceptor-specific effects of β-ionone. To test the two hypotheses, we applied β-ionone to partially bleached blue-sensitive rods and cones of salamander, two cells that couple the same cone-like opsin to either rod or cone transducin, respectively. Immunocytochemistry confirmed that all salamander rods contain one form of transducin, whereas all cones contain another. β-Ionone enhanced pigment adaptation in blue-sensitive rods, but it also did so in blue- and UV-sensitive cones. Furthermore, all recombinant salamander rod and cone opsins, with the exception of the red-sensitive cone opsin, activated rod transducin upon the addition of β-ionone. Thus opsin structure determines the identity of β-ionone as an agonist or an inverse agonist and in that respect distinguishes the red-sensitive cone opsin from all others.

Calcium (Ca2+) is thought to play a major role in the photoresponse of both vertebrates and invertebrates, but the mechanisms through which Ca2+ exerts its effects are unclear. In many systems, some effects of Ca2+ on cellular processes are thought to be mediated via activation of calcium/calmodulin protein kinase (CaCAM-PK) and the phosphorylation of specific proteins. Thus, protein substrates for CaCAM-PK in photoreceptor cells may be important in mediating the effects of Ca2+ on the photoresponse.

In this study, we identify eight substrates for CaCAM-PK found in both the ventral and lateral eyes of Limulus. We focus on a characterization of one of these, a 46-kD substrate. We show that its subcellular distribution in ventral photoreceptors and its isoelectric forms are identical to the 46-kD light-stimulated phosphoprotein (46A) described by Edwards et al. (1989). Furthermore, we present evidence that 46A is unique to photoreceptor cells, and that it is present throughout the cell. Based on the results of this study, and the previous study by Edwards et al. (1989), we propose that 46A is involved in mediating the effects of Ca2+ on Limulus photoreceptor cell function, and that it may be involved in dark adaptation.

Monocular deprivation in adult macaques produces a rapid down-regulation in GABA and GABAA receptor subunit immunoreactivity in deprived-eye columns of primary visual cortex (V1) but a significantly delayed GABA reduction in deprived layers of the dorsal lateral geniculate nucleus (LGN). These findings, suggesting that normal inhibitory neurotransmission persists in LGN at a time when V1 inhibitory mechanisms are greatly altered, are consistent with physiological studies that have demonstrated a greater degree of functional plasticity in V1 than in LGN. Nonetheless, functional adaptation to partial loss of visual input has been detected in the LGN, indicating that synaptic plasticity takes place in this nucleus. In the present study, evidence for early changes in inhibitory neurotransmission were examined with immunocytochemical methods to determine if, in the absence of early GABA regulation, GABAA receptor subunits in macaque LGN are affected by adult deprivation. Immunoreactivity for α1 and β2/3 subunits of the GABAA receptor was intense within the magnocellular layers and more modest in the parvocellular layers and intercalated layers. In all layers, immunoreactivity was present in the cytoplasm and along the surfaces of relatively large somata and in dense tangles of processes in the neuropil. Double-labeling experiments demonstrated that somata and processes immunoreactive for α 1 and β2/3 were surrounded by GABA terminals but no cell intensely immunoreactive for either subunit expressed immunoreactivity for GABA, itself. Following periods of monocular deprivation by tetrodotoxin (TTX) injection for 4 days or longer, layers deprived of visual activity displayed levels of α 1 and β2/3 immunoreactivity markedly lower than those displayed by the adjacent, normally active layers. Such changes were greater as the period of deprivation increased. The changes included a loss of immunostaining in and around somata and in many neuropil elements of deprived layers. These data indicate that GABA and GABAA receptor subunits α 1 and β2/3 are expressed by separate populations of neurons in macaque LGN that are differentially regulated by visual activity. The findings suggest that rapid, activity-dependent regulation of postsynaptic receptors represents one mechanism for altering synaptic strength in the adult macaque visual system.

Neurons of the horizontal cell retinal neural network are subject to modulation by the neurotransmitter nitric oxide (NO). We have examined the effects of NO on glutamate receptor function in isolated horizontal cells from the perch (Perca fluviatilis) using the concentration ramp technique to simultaneously record receptor current and agonist concentration. Dose–response curves for glutamate (0–1 mM) and kainate (0–200 μM) were measured in the presence and absence of 1–2 mM sodium nitroprusside (SNP), 1 mM 8-Br-cGMP, 100 μM cyclothiazide or 200 μM dopamine as modulators. SNP increased the EC50 (i.e. decreased affinity) for glutamate and increased Imax (i.e. increased efficacy), whereas 8-Br-cGMP increased EC50, but not Imax. In the presence of the α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptor desensitization blocker cyclothiazide, the SNP-induced increase in EC50 persisted, but the increase in Imax was blocked. The increase in EC50, but not the increase in Imax, was also observed when the non-desensitizing agonist kainate (100–200 μM) was applied in the presence of SNP. When 2 mM SNP and 200 μM dopamine were applied together, they increased Imax (740 vs. 2455 pA) and EC50 (422 vs. 682 μM). Our findings indicate that NO modulates horizontal cell glutamate responses by reducing the affinity of receptors for glutamate while simultaneously increasing the maximal current. The shift in affinity is cGMP-mediated and independent of desensitization. The action of NO on horizontal cell glutamate receptors is distinct from, but synergistic with, that of dopamine. Glutamate receptor modulation by NO qualitatively predicts the action of NO on horizontal cell light responses in situ and may alter transmission at visual synapses according to adaptational conditions.

The P23H-1 transgenic rat carries a mutated mouse opsin gene, in addition to endogenous opsin genes, and undergoes progressive photoreceptor loss that is generally characteristic of human autosomal dominant retinitis pigmentosa (RP). Here, we examined morphological changes correlated with visual function that is comparable to clinical application in the pigmented P23H-1 rat retina as photoreceptor degeneration progressed. We found that rod function was compromised as early as postnatal day 28 and was a good indicator for tracking retinal degeneration. Cone function was normal and did not change until the thickness of the photoreceptor layer was reduced by 75%. Similar to the threshold versus intensity curves used to evaluate vision of RP patients, light-adaptation curves showed that cone thresholds depended on the number of remaining functioning cones, but not on its length of outer segments (OS). By 1 year of age, both rod and cone functions were significantly compromised. Correlating with early abnormal rod function, rods and related secondary neurons also underwent progressive degeneration, including shortening of inner and OS of photoreceptors, loss of rod bipolar and horizontal cell dendrites, thickening of the outer Müller cell processes, and reduced density of pre- and postsynaptic markers. Similar early morphological modifications were also observed in cones and their related secondary neurons. However, cone function was maintained at nearly normal level for a long period. The dramatic loss of rods at late stage of degeneration may contribute to the dysfunction of cones. Attention has to be focused on preserving cone function and identifying factors that damage cones when therapeutic regimes are applied to treat retinal degeneration. As such, these findings provide a foundation for future studies involving treatments to counter photoreceptor loss.

A number of authors have observed amacrine cells containing high levels of immunoreactive parvalbumin in primate retinas. The experiments described here were designed to identify these cells morphologically, to determine their neurotransmitter, to record their light responses, and to describe the other cells that they contact. Macaque retinas were fixed in paraformaldehyde and labeled with antibodies to parvalbumin and one or two other markers, and this double- and triple-labeled material was analyzed by confocal microscopy. In their morphology and dendritic stratification patterns, the parvalbumin-positive cells closely resembled the knotty type 2 amacrine cells described using the Golgi method in macaques. They contained immunoreactive glycine transporter, but not immunoreactive γ-aminobutyric acid, and therefore, they use glycine as their neurotransmitter. Their spatial density was relatively high, roughly half that of AII amacrine cells. They contacted lobular dendrites of AII cells, and they are expected to be presynaptic to AII cells based on earlier ultrastructural studies. They also made extensive contacts with axon terminals of OFF midget bipolar cells whose polarity cannot be predicted with certainty. A macaque amacrine cell of the same morphological type depolarized at the onset of increments in light intensity, and it was well coupled to other amacrine cells. Previously, we described amacrine cells like these that contacted OFF parasol ganglion cells and OFF starburst amacrine cells. Taken together, these findings suggest that one function of these amacrine cells is to inhibit the transmission of signals from rods to OFF bipolar cells via AII amacrine cells. Another function may be inhibition of the OFF pathway following increments in light intensity.

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.

The ommatidia of the lateral eye of the horseshoe crab, Limulus polyphemus, undergo rhythmic changes in structure that are driven by diurnal lighting and efferent neural activity from a circadian clock in the brain. This study uses cytochemical probes to investigate the cytoskeletal elements mediating these responses and to develop models for their control. Antibodies to actin and phalloidin, a specific F-actin probe, label the rhabdom of lateral eye ommatidia, the cone cells of the ommatidial aperture, the ommatidial sheath, and the peripheral regions of the photoreceptor (retinular cell) cytoplasm. These probes also label the rhabdomere of ventral photoreceptors. Antibodies to tubulin label the eccentric cell dendrite and soma in each lateral eye ommatidium, the cone cells of the aperture, and the peripheral retinular cell cytoplasm. Models are proposed for the cytoskeletal mechanisms involved in controlling aperture and rhabdom shape, pigment movement, and shedding of rhabdomeral membrane.

The Farnsworth D15 test (D15) was developed for use in occupational guidance. People with significant color deficiency, including all dichromats are expected to fail and people with slight color deficiency are expected to pass. Pass is a circular results diagram and fail an interlacing pattern with one or more red-green isochromatic errors (Farnsworth, 1947). The Nagel anomaloscope is a “gold standard” reference test for identifying and classifying red-green color deficiency. The matching range on the red/green mixture scale indicates the severity of the discrimination deficit. Pass/fail results for the D15 are presented for 107 protanomalous and 410 deuteranomalous trichromats and compared with the anomaloscope matching range. Thirty-six percent of the subjects examined failed the D15. Protanomalous trichromats are able to utilize perceived luminance contrast to obtain good results on the D15 but 42% of these subjects failed the D15 compared with 35% of deuteranomalous subjects. Failure of the D15 was clearly related to the Nagel matching range in deuteranomalous trichromatism but not in protanomalous trichromatism. For example, 84% of deuteranomalous subjects with matching ranges > 30 scale units failed the D15 but only 2% with matching ranges < 9 scale units were unsuccessful. In comparison, 53% of protanomalous subjects with matching ranges > 15 scale units and 33% of subjects with matching ranges < 5 scale units were unsuccessful. Protanomalous trichromats with apparently minimal color deficiency are therefore shown to have poor practical hue discrimination ability as measured with this test.

Ultrastructural examination of photoreceptor inner segment ellipsoids in larval (4, 8, and 15 days postfertilization; dpf) and adult zebrafish identified morphologically different types of mitochondria. All photoreceptors had mitochondria of different sizes (large and small). At 4 dpf, rods had small, moderately stained electron-dense mitochondria (E-DM), and two cone types could be distinguished: (1) those with electron-lucent mitochondria (E-LM) and (2) those with mitochondria of moderate electron density. These distinctions were also apparent at later ages (8 and 15 dpf). Rods from adult fish had fewer mitochondria than their corresponding cones. The ellipsoids of some fully differentiated single and double cones contained large E-DM with few cristae; these were surrounded by small E-LM with typical internal morphology. The mitochondria within the ellipsoids of other single cones showed similar electron density. Microspectrophotometry of cone ellipsoids from adult fish indicated that the large E-DM had a small absorbance peak (∼0.03 OD units) and did not contain cytochrome-c, but crocetin, a carotenoid found in old world monkeys. Crocetin functions to prevent oxidative damage to photoreceptors, suggesting that the ellipsoid mitochondria in adult zebrafish cones protect against apoptosis and function metabolically, rather than as a light filter.

To study the relationship between ocular dominance columns (ODCs) and axonal projections of individual layer 6 pyramidal neurons in the primary visual cortex, neurons were intracellularly labeled with biocytin in live slices prepared from macaque monkeys that had received an intravitreal injection of tetrodotoxin (TTX). The TTX injection indirectly causes a decrease in cytochrome oxidase (CO) expression in the cortical ODCs corresponding to the treated eye (Wong-Riley & Carroll, 1984). Sections from slices with labeled layer 6 neurons were double stained for biocytin and CO, to allow visualization of neuronal processes as well as ODCs. Twenty-seven layer 6 pyramidal neurons in ODC-labeled slices were analyzed. These neurons were classified according to the criteria of Wiser and Callaway (1996). Eight of these are class I neurons, which have dense axonal projections to the monocular layer 4C. The remaining 19 are class II neurons which project primarily to the binocular layers outside 4C. Among class I neurons, two have dense axonal arbors in layer 4Cα (type Iα), one in layer 4Cβ (type Iβ), and two throughout the depth of layer 4C (type IC). None of these neurons have ODC-specific axonal arbors. The remaining three class I neurons have focused axonal projections in layers 4Cβ and 4A (type IβA). All three appear to have axonal arbors predominantly within their home ODC in layer 4C. The axonal arbors of class II neurons do not appear to relate to ODCs in any specific fashion.

In the marmoset Callithrix jacchus, ocular dominance columns (ODC) have been reported to be present in young animals, but absent in adults (Spatz, 1989). We have studied in juvenile and adult animals the postnatal organization of the retino-geniculo-cortical afferents by means of transneuronal labeling. We show in the present work that ODC are present in the primary visual cortex of Callithrix jacchus, both in the adult and in the juvenile animal. The present work confirms the presence of ODC in the visual cortex of juvenile marmoset before the end of the first postnatal month. In 2-month-old animals, ODC are well demarcated in IVcα and IVcβ. In the adult marmosets, the present data clearly show that the primary visual cortex is also organized with ODC. In horizontal sections, they form a mosaic through the ventral and dorsal calcarine cortex and through the dorso-lateral occipital part of the striate cortex. In frontal sections, their presence is manifest in IVcβ within the calcarine cortex and they only faintly appear in IVcα. These new findings are important since they underline the usefulness of the adult New World Monkeys as a model in visual research.