The goals of these experiments were to describe the morphology and synaptic connections of amacrine cells in the baboon retina that contain immunoreactive vesicular glutamate transporter 3 (vGluT3). These amacrine cells had the morphology characteristic of knotty bistratified type 1 cells, and their dendrites formed two plexuses on either side of the center of the inner plexiform layer. The primary dendrites received large synapses from amacrine cells, and the higher-order dendrites were both pre- and postsynaptic to other amacrine cells. Based on light microscopic immunolabeling results, these include AII cells and starburst cells, but not the polyaxonal amacrine cells tracer-coupled to ON parasol ganglion cells. The vGluT3 cells received input from ON bipolar cells at ribbon synapses and made synapses onto OFF bipolar cells, including the diffuse DB3a type. Many synapses from vGluT3 cells onto retinal ganglion cells were observed in both plexuses. At synapses where vGluT3 cells were presynaptic, two types of postsynaptic densities were observed; there were relatively thin ones characteristic of inhibitory synapses and relatively thick ones characteristic of excitatory synapses. In the light microscopic experiments with Neurobiotin-injected ganglion cells, vGluT3 cells made contacts with midget and parasol ganglion cells, including both ON and OFF types. Puncta containing immunoreactive gephyrin, an inhibitory synapse marker, were found at appositions between vGluT3 cells and each of the four types of labeled ganglion cells. The vGluT3 cells did not have detectable levels of immunoreactive γ-aminobutyric acid (GABA) or immunoreactive glycine transporter 1. Thus, the vGluT3 cells would be expected to have ON responses to light and make synapses onto neurons in both the ON and the OFF pathways. Taken with previous results, these findings suggest that vGluT3 cells release glycine at some of their output synapses and glutamate at others.

Quantitative light and electron microscopy was used to monitor the extent of retinal degeneration as a function of age and temperature in the white-eyed rdgBKS222 mutant of Drosophila melanogaster. Parallel measurements of the electroretinogram (ERG) of the degenerating retina reveal a new phenomenon – the appearance of spike potentials following illumination with bright light. These spikes, which do not appear in the normal fly retina, have a relatively long duration (20–50 ms), regenerative properties, and a rate of occurrence which increases with increasing light intensity. The spikes differed from the light response in being more susceptible to CO2 and to cuts in the eye. The spikes completely disappeared at low extracellular Ca2+ levels which did not reduce the amplitude of the light response. The spike potentials become triphasic when the recording electrode is advanced to the level of the basement membrane. This suggests that the spike potentials originate from the photoreceptor axons as a result of synchronous opening of voltage-dependent channels in a large number of photoreceptor cells. The occurrence of spike potentials during the process of degeneration was studied. Two phases can be distinguished: (1) Spike potentials appear in retinae of 2–3-day-old flies which display few morphological signs of degeneration. The frequency of appearance of spike potentials decreases in retinae of 14–16-day-old flies which show extensive degeneration of the R1–6 photoreceptor cells but no degeneration of the central R7,8 cells. (2) Spike potentials appear more frequently again in flies of 22–24 d of age. This is probably a consequence of degeneration of the remaining R7,8 photoreceptor cells. Temperature and the light-dark cycle had a critical effect on degeneration. Eight-day-old mutants raised at 19°C in a normal light-dark cycle showed only little degeneration. Eight-day-old mutants raised at 24°C showed only a slight degeneration when raised in the dark. However, the degree of degeneration was greatly enhanced in the mutants raised at 24°C under a light-dark cycle regime.

The combined electrophysiological and morphological study of the degeneration, as a function of age and temperature, revealed that (1) the degeneration process takes place even in darkness, but at a slow rate, while light greatly accelerates the degeneration. (2) The degeneration is negligible at 19°C, even during light, in the first week after eclosion. (3) The appearance of spike potentials at an early stage of the degeneration suggests that changes in the plasma membrane of the photoreceptor cells manifest at an initial stage of the degeneration process.

Different types of retinal ganglion cell show differences in their response properties. Here we investigated the question of whether these differences are related to the distribution of the synaptic input to the dendritic tree. We measured the distribution and density of synaptic input to the dendrites of midget and parasol ganglion cells in the retina of a New World monkey, the marmoset, Callithrix jacchus. Ganglion cells were retrogradely labeled by dye injection into parvocellular or magnocellular regions of the lateral geniculate nucleus and subsequently photo-filled. Presumed bipolar cell synapses were identified immunocytochemically using antibodies against the ribbon protein CtBP2 or the GluR4 subunit of the AMPA receptor. For all cells, colocalized immunoreactive puncta were distributed across the entire dendritic tree. The density of the presumed bipolar input to midget ganglion cells was comparable for both synaptic markers, suggesting that the AMPA receptor GluR4 subunit is expressed at all synapses between midget bipolar and midget ganglion cells. Midget ganglion cells had an average of nine colocalized immunoreactive puncta per 100 μm2 dendritic surface, and parasol cells had an average of seven colocalized immunoreactive puncta per 100 μm2 dendritic surface. The densities were comparable in different regions of the dendritic tree and were not influenced by the location of the cells with respect to the fovea. Our findings suggest that the differences in the response characteristics of midget and parasol cells are not due to differences in the density of synaptic input to their dendritic tree.

The compound lateral eye of the adult horseshoe crab, Limulus polyphemus, views the world with approximately 1000 ommatidia. Their optical properties and orientation determine the eye's resolution, field of view, and light collecting ability. Optic axes of adjacent ommatidia diverge from 1–15 deg with an average value of 5.5 deg yielding an average resolution of 0.1 cycles/deg. Resolution is not uniform across the eye: along horizontal planes, it is maximal in the anterior region of the eye (0.22 cycle/deg) and minimal in the posterior region (0.07 cycle/deg); along vertical planes, it is maximal near or just below the horizon (0.23 cycle/deg) and minimal above the horizon (0.04 cycle/deg). Together the ommatidia of one eye view approximately 60% of the hemispheric world on one side of the body. There is little binocular overlap (<1% of total field). Ommatidial facets of up to 320 μm in diameter (among the largest known in the animal kingdom) make the eye a superb light collector. Limulus are known to use vision to find mates both day and night. Apparently, the optics of the lateral eye sample a large enough part of the world with sufficient resolution and light-collecting ability for the animal to succeed at this essential task.

Most of the blinding retinopathies are due to progressive photoreceptor degeneration. Treatment paradigms that are currently being investigated include strategies to either halt or slow down photoreceptor cell loss, or to replace useful vision with retinal prosthesis. However, more information is required on the pathophysiological changes of the diseased retina, in particular the inner retina, that occur as a consequence of photoreceptor cell loss. Here we wished to use light damage as a stoppable insult to determine the structural and functional consequences on inner and outer retina, with the overall goal of determining whether survival of a functional inner retina is possible even if the outer retina is damaged. Mice were exposed to a 20-day light-damage period. Electroretinograms (ERG) and morphology were used to assess subsequent recovery. Outer retina was monitored analyzing a-waves, which represent photoreceptor cell responses, and histology. Integrity of the inner retina was monitored, analyzing b-waves and oscillatory potentials (OP1–OP4) and immunohistochemical markers for known proteins of the inner retina. All six ERG components were significantly suppressed with respect to amplitudes and kinetics, but stabilized in a wave-dependent manner within 40–70 days after the end of light exposure. As expected, damage of the outer retina was permanent. However, function of the inner retina was found to recover significantly. While b-wave amplitudes remained suppressed to 60% of their baseline values, OP amplitudes recovered completely, and implicit times of all components of the inner retina (b-wave and OP1–OP4) recovered to a level close to baseline values. Histological analyses confirmed the lack of permanent damage to the inner retina. In summary, these data suggests that the inner retina has the potential for significant recovery as well as plasticity if treatment is available to stop the deterioration of the outer retina.

The visual cortex of freshwater turtles contains pyramidal cells, which have a regular spiking (RS) firing pattern, and several categories of aspiny, inhibitory interneurons. The interneurons show diverse firing patterns, including the fast spiking (FS) pattern. Postsynaptic potentials (PSPs) evoked in FS cells by visual stimulation of the retina reach their peak amplitudes as much as 200 ms before PSPs in RS cells (Mancilla et al., 1998). FS cells could, consequently, control the amplitudes of light-evoked PSPs in RS cells by producing disynaptic, feedforward inhibitory postsynaptic potentials (IPSPs) that overlap in time with geniculocortical excitatory postsynaptic potentials (EPSPs). Since FS cells receive recurrent, excitatory inputs from RS cells, they could also control the amplitudes of light-evoked PSPs in RS cells via polysynaptic, feedback inhibition. The in vitro geniculocortical preparation of Pseudemys scripta was used to characterize the temporal relationships of EPSPs and IPSPs produced in RS cells by electrical activation of geniculate afferents and by diffuse light flashes presented to the retina. GABAA receptor-mediated inhibition was blocked using extracellular application of bicuculline (3.5 mM) or intracellular perfusion of picrotoxin (1 μM) in individual RS cells. Electrical stimulation of thalamic afferents produced compound PSPs. Blockade of GABAA receptor-mediated IPSPs with either bicuculline or picrotoxin provided evidence for both early and late IPSPs in RS cells. Analysis of the apparent reversal potentials of light-evoked PSPs indicated the existence of early IPSPs during the first 140–300 ms following light onset. Light responses of cells perfused with picrotoxin diverged from control light responses at about 300 ms after light onset and had maximum amplitudes that were significantly different from control light responses. These experiments indicate that the responses of RS cells to both electrical and natural stimulation of geniculate afferents are controlled by both early and late IPSPs, consistent with activation of both feedforward and feedback pathways.

Most animals experience daily changes in light and darkness. The retinas of many of these animals show concomitant rhythmic changes in the levels of mRNAs that encode proteins involved in the photoresponse. These changes may be circadian and independent of light, independent of circadian clocks and regulated by light, or regulated by a circadian clock and light. We have taken advantage of the organization of the Limulus visual system to examine the separate and combined effects of signals from a circadian clock and light on arrestin mRNA levels in photoreceptors. The clock that regulates photoreceptors in the lateral eye of Limulus is in the brain, and signals from the clock reach the lateral eye via activation of a well-characterized efferent projection in the lateral optic nerve. In the experiments described, clock-driven efferent input to the lateral eye was eliminated by cutting the lateral optic nerve, and light input to the lateral eye was eliminated by placing an opaque patch over the eye. Arrestin mRNA levels were quantified relative to 18s rRNA with a ribonuclease protection assay. We observed the following. In lateral eyes exposed to natural diurnal light and endogenous efferent nerve activity, the level of arrestin mRNA was higher during the day in the light than during the night in the dark. Circadian efferent nerve activity was necessary and sufficient to produce normal daily fluctuations in the level of arrestin mRNA. Light influenced arrestin mRNA levels only in eyes with intact and active efferent projections. We conclude that arrestin mRNA levels in lateral eye photoreceptors are controlled entirely by efferent nerve activity, and that light exerts its effects by modulating this output from the circadian clock. Light-stimulated changes in arrestin mRNA in the vertebrate retina may likewise require interactions between light-driven biochemical cascades and clock output.

Calcium ion (Ca2+) signaling has been widely implicated in developmental events in the retina, but little is known about the specific mechanisms utilized by developing neurons to decrease intracellular Ca2+. Using immunocytochemistry, we determined the expression profiles of all known isoforms of a key Ca2+ transporter, the plasma membrane Ca2+ ATPase (PMCA), in the rat retina. During the first postnatal week, the four PMCA isoforms were expressed in patterns that differed from their expression in the adult retina. At birth, PMCA1 was found in the ventricular zone and nascent cell processes in the distal retina as well as in ganglion and amacrine cells. After the first postnatal week, PMCA1 became restricted to photoreceptors and cone bipolar cells. By P10 (by postnatal day 10), most inner retinal PMCA consisted of PMCA2 and PMCA3. Prominent PMCA4 expression appeared after the first postnatal week and was confined primarily to the ON sublamina of the inner plexiform layer (IPL). The four PMCA isoforms could play distinct functional roles in the development of the mammalian retina even before synaptic circuits are established. Their expression patterns are consistent with the hypothesis that inner and outer retinal neurons have different Ca2+ handling needs.

We have previously reported that the responses of individual neurons in macaque visual area MT elicited by movement of contrast-reversing heterochromatic red/green borders are largest when the two hues are “balanced” or isoluminant (Dobkins & Albright, 1994). This “neural” isoluminant point was found to vary somewhat across the sample of neurons. Here, we compare the average neural isoluminant point in area MT to a behavioral measure of isoluminance, obtained using a modification of an oculomotor procedure developed by Chaudhuri and Albright (1992). These behavioral estimates of isoluminance closely parallel the neuronal data obtained from area MT. In accordance with previous evidence (e.g. Lee et al., 1988; Kaiser et al., 1990; Valberg et al., 1992), this correlation suggests that activity within the dorsal/magnocellular stream underlies behavioral expression of chromatic isoluminance.

The responsiveness of luminosity-type horizontal cells, recorded intracellularly from isolated hybrid bass retinas, decreased after superfusion for 2 h in constant darkness. Responsiveness was subsequently increased (light-sensitized) up to 10-fold after exposure to several short (~0.5 min) periods of continuous illumination. The increase in horizontal cell responsiveness following light-sensitization was due to an increase of peak response amplitude rather than a reduction of peak response time. The increased responsiveness after light-sensitization was intensity-dependent with brighter sensitizing stimuli causing a greater increase than dimmer stimuli. The extent of LHC dark-suppression was affected by the time of day, being greater when induced during the night than during the day. However, there was no significant difference in horizontal cell responsiveness after light-sensitization in retinas studied during the night compared to those studied during the day The responsiveness of light-sensitized horizontal cells from isolated hybrid bass retinas was found to be suppressed by relatively brief periods of darkness. The responsiveness of horizontal cells, that were first light-sensitized, decreased by more than 50% following only 5 min of darkness. Suppression of light-sensitized horizontal cell responsiveness after such a short time in the dark has not been described in other teleost retinas. The suppression of light-sensitized horizontal cell responsiveness in hybrid bass retinas may be rapid in comparison to other teleosts.

In human subjects, the blind spot is perceptually filled-in by color and brightness from the surrounding visual field. The present behavioral study examined the occurrence of color filling-in at the blind spot in monkeys. First, the location of the blind spot was determined using a monocular saccade task. The blind spots were located on the horizontal meridian at approximately 15–17 deg from the fixation point in the temporal visual field. Then, filling-in at the blind spot was tested by determining if the monkey could discriminate between an annulus presented on the blind spot and a homogeneous disk in the normal visual field. In this task, the monkey was required to make a saccade to a homogeneous disk of the same color and size as an annulus presented simultaneously in the opposite field. Both stimuli were large enough to cover the blind spot and the inner circle of the annulus was confined inside the blind spot. All four monkeys tested performed this task correctly in over 80% of the trials. However, when one eye was covered and the annulus was presented on the blind spot of the uncovered eye, performance deteriorated significantly. To confirm that these results reflected filling-in, one monkey was trained to maintain fixation when two identical homogeneous disks appeared in opposite visual fields. When only one eye was uncovered, and the annulus was presented on the blind spot of the uncovered eye, the monkey maintained fixation in most of the trials. These results show that monkeys were unable to distinguish an annulus from a homogeneous disk when the annulus was presented on the blind spot. This indicates that color filling-in occurs at the blind spot in monkeys and opens possibility to physiological experiments to study the neural mechanisms of filling-in.

We performed genome-wide mutagenesis of C57BL/6J mice using the mutagen N-ethyl-N-nitrosourea (ENU) and screened the third generation (G3) offspring for visual system alterations using electroretinography and fundus photography. Several mice in one pedigree showed characteristics of retinal degeneration when tested at 12–14 weeks of age: no recordable electroretinogram (ERG), attenuation of retinal vessels, and speckled pigmentation of the fundus. Histological studies showed that the retinas undergo a photoreceptor degeneration with apoptotic loss of outer nuclear layer nuclei but visual acuity measured using the optomotor response under photopic conditions persists in spite of considerable photoreceptor loss. The Noerg-1 mutation showed an autosomal dominant pattern of inheritance in progeny. Studies in early postnatal mice showed degeneration to occur after formation of partially functional rods. The Noerg-1 mutation was mapped genetically to chromosome 6 by crossing C57BL/6J mutants with DBA/2J or BALB/cJ mice to produce an N2 generation and then determining the ERG phenotypes and the genotypes of the N2 offspring at multiple loci using SSLP and SNP markers. Fine mapping was accomplished with a set of closely spaced markers. A nonrecombinant region from 112.8 Mb to 115.1 Mb was identified, encompassing the rhodopsin (Rho) coding region. A single nucleotide transition from G to A was found in the Rho gene that is predicted to result in a substitution of Tyr for Cys at position 110, in an intradiscal loop. This mutation has been found in patients with autosomal dominant retinitis pigmentosa (RP) and results in misfolding of rhodopsin expressed in vitro. Thus, ENU mutagenesis is capable of replicating mutations that occur in human patients and is useful for generating de novo models of human inherited eye disease. Furthermore, the availability of the mouse genomic sequence and extensive DNA polymorphisms made the rapid identification of this gene possible, demonstrating that the use of ENU-induced mutations for functional gene identification is now practical for individual laboratories.

There are four types of horizontal cell in the goldfish retina, three cone- and one rod-type. The neurotransmitter of only one type, the H1 (cone) horizontal cell, has been identified as GABA. 3H-adenosine uptake was examined as a possible marker for the other classes of horizontal cell. Isolated goldfish retinae were incubated in 3H-adenosine (10–40 μCi) in HEPES-buffered saline for 30 min, then fixed, embedded in plastic, and processed for light-microscopic autoradiography (ARG). For double-label immuno/ARG studies, l-μm-thick sections were processed for GABA postembed immunocytochemistry, then for ARG. 3H-adenosine uptake was localized to cone photoreceptors, presumed precursor cells in the proximal outer nuclear layer, and to a single, continuous row of horizontal cell bodies in the inner nuclear layer. No uptake was localized to the region of horizontal cell axon terminals. 3H-adenosine uptake did not colocalize with GABA-IR in H1 horizontal cells, but it did colocalize with adenosine deaminase immunoreactivity. It is concluded that 3H-adenosine uptake selectively labels rod horizontal cells in the goldfish retina based on position and staining pattern, which are similar to rod horizontal cells stained by Golgi or HRP injection methods. The use of 3H-adenosine uptake may provide a useful tool to study other properties of rod horizontal cells (i.e. development) as well as provide clues as to the transmitter used by these interneurons.

It is implicit in many cone-specific ERG studies that the amplitude is proportional to the numbers of cones stimulated. The objective of these experiments was to test this idea by comparing ERGs obtained from different areas of the retina with histological data on cone-density distributions. The histology (Curcio et al., 1990) shows that the cumulative number of cones in the human retina increases exponentially with stimulus diameter between 0- and 40-deg eccentricity. L-, M-, and (L+M) cone-driven 30-Hz ERGs were obtained from a series of stimuli with one of the following configurations: (1) Circular stimuli of different angular subtense up to 70-deg diameter. (2) Annuli with 70-deg outer diameter but variable inner diameter. (3) Annuli of constant area but increasing eccentricity. Cone contrasts were equalized for each stimulus condition. The modulated and nonmodulated regions of the screen had the same mean hue and luminance. The data suggest that the L+M cone ERG amplitude increases with stimulus diameter in direct proportion to the estimated number of cones stimulated. Furthermore, the total L+M responses appear to be predicted from individual L and M responses by simple linear summation for both the disc and annular stimuli.

Centrifugal modulation of visual responsiveness of tectal cells by the isthmo-optic nucleus (ION) through the retina was studied in homing pigeons. Visual activity evoked by computer-generated stimuli was reduced by an average of 59% in tectal cells whose receptive fields (RFs) either overlapped with, or were close to, those of isthmo-optic cells whose activity was blocked by the injection of lidocaine through micropipettes. Activity usually recovered to 87% of pre-drug controls in 8–17 min (average 12.3 min) after stopping lidocaine injections. Those tectal cells whose RFs were far from those of ION cells did not show clear-cut changes in their visual responsiveness to isthmo-optic lidocaine application. The spatial relationship between receptive fields of tectal and isthmo-optic cells, saline controls, as well as the specificity, reproducibility and reversibility of effects of ION-injected lidocaine on tectal activity, show that this chemical action is pharmacological, not toxicological. Neuronal circuitry underlying centrifugal modulation of tectal activity by isthmo-optic cells is discussed.

Impulse response functions (IRFs) were obtained from two-pulse detection thresholds using isoluminant stimuli that produced increments or decrements in S-cone excitation. The pulses were chromatically modulated at constant luminance (based on 18 Hz heterochromatic flicker photometry). Chromatic stimuli were presented as a Gaussian patch (±1 SD = 2.3°) in one of four quadrants around a central fixation cross on a CRT screen. Each of the two pulses (6.67 ms) was separated by an inter-stimulus interval (ISI) from 20 to 360 ms. Chromaticity of the pulses was changed from the equal-energy white of the background to a bluish or yellowish color along individually determined tritan lines (based on color matching under strong S-cone adaptation from a 420 nm background superimposed in Maxwellian view). Chromatic detection thresholds were determined by a four-alternative forced-choice method with staircases for each ISI interleaved in each session. Measurements were repeated in at least four sessions for each observer. IRFs were calculated by varying four parameters of an exponentially-damped sinewave. Both S-cone increment and decrement IRFs are characterized by a single excitatory phase and a much longer time course compared with IRFs derived for luminance modulation using the same apparatus and observers. S-cone increment IRFs are faster than S-cone decrement IRFs; the time to peak amplitude of S-cone increment and decrement IRFs is 50–70 and 100–120 ms, respectively. These results were used to derive the temporal contrast sensitivity for human observers of putative ON- and OFF-channels carrying signals from S-cones.

We examined the numerical correlation between total populations of neurons in the lateral geniculate nucleus (LGN) and the primary visual cortex (area 17 of Brodmann) in ten cerebral hemispheres of five normal rhesus monkeys using an unbiased three-dimensional counting method. There were 1.4 ± 0.2 million and 341 ±54 million neurons in the LGN and area 17, respectively. In each animal, a larger LGN on one side was in register with a larger area 17 of the cortex on the same side. Furthermore, asymmetry in the number of neurons in both the LGN and area 17 favored the right side. However, because of small variations across subjects, correlation between the total neuron number in LGN and area 17 was weak (r = 0.29). These results suggest that the final numbers of neurons in these visual centers may be established independently or by multiple factors controlling elimination of initially overproduced neurons.

This study investigates the receptive-field structure of mechanisms operating in human color vision, by recording visual evoked potentials (VEPs) to multiharmonic gratings modulated either in luminance or color (red-green). Varying the Fourier phase of the harmonics from 0 deg to 90 deg produced a family of stimulus profiles that varied from lines to edges. The stimuli were contrast reversed to elicit steady-state VEPS, and also randomly jittered (at a higher temporal frequency than the contrast reversal) to ensure that the evoked response resulted from the polarity reversal, rather than from local variation of luminance or color. Reliable VEPs were recorded from both luminance and chromatic stimuli at all phases, suggesting that the mechanisms sensitive to chromatic contrast and those sensitive to luminance contrast have both symmetric and asymmetric receptive fields. Contrast thresholds estimated by extrapolation of the contrast response curves were very similar to psychophysical thresholds for phase discrimination, suggesting that the VEP response is generated by mechanisms mediating phase discrimination. The results support the idea that human color mechanisms have receptive fields with a variety of spatial symmetries (including odd- and even-symmetric fields) and that these mechanisms may contribute to phase discrimination of chromatic stimuli in a similar way to what has been suggested for luminance vision.

The dendritic form of a cell may be established by many factors both intrinsic and environmental. Blockade of action potentials along the course of axons and in their postsynaptic targets dramatically alters the development of axonal morphology. The extent to which blockade of target cell activity retrogradely alters the dendritic morphology of the presynaptic cells is unknown. To determine whether the establishment of dendritic form by developing retinal canclion cells depends on activity within their targets, the sodium channel blocker, tetrodotoxin (TTX), was administered via minipumps to the diencephalon of cat fetuses from embryonic day 43 (E43) to E57. At E57 retinae were removed and living retinal ganglion cells injected in vitro with Lucifer yellow to reveal their dendritic morphology. In the TTX-treated animals both alpha and beta types of retinal ganglion cells were present, as were putative gamma cells. Overall, the dendrites of retinal ganglion cells in TTX-treated animals appeared qualitatively and Quantitatively similar to those of untreated animals. The only significant change in the TTX-treated cases was a small increase in the number of dendritic spines on the non-beta cells. These results indicate that the acquisition of basic dendritic form of developing ganglion cells is not influenced by the action potential activity within their targets, and that it is also independent of the terminal branching patterns of their axons.

In primates, the cortex adjoining the rostral border of V2 has been variously interpreted as belonging to a single visual area, V3, with dorsal V3 (V3d) representing the lower visual quadrant and ventral V3 (V3v) representing the upper visual quadrant, V3d and V3v constituting separate, incomplete visual areas, V3d and ventral posterior (VP), or V3d being divided into several visual areas, including a dorsomedial (DM) visual area, a medial visual area (M), and dorsal extension of VP (or VLP). In our view, the evidence from V1 connections strongly supports the contention that V3v and V3d are parts of a single visual area, V3, and that DM is a separate visual area along the rostral border of V3d. In addition, the retinotopy revealed by V1 connection patterns, microelectrode mapping, optical imaging mapping, and functional magnetic resonance imaging (fmri) mapping indicates that much of the proposed territory of V3d corresponds to V3. Yet, other evidence from microelectrode mapping and anatomical connection patterns supports the possibility of an upper quadrant representation along the rostral border of the middle of dorsal V2 (V2d), interpreted as part of DM or DM plus DI, and along the midline end of V2d, interpreted as the visual area M. While the data supporting these different interpretations appear contradictory, they also seem, to some extent, valid. We suggest that V3d may have a gap in its middle, possibly representing part of the upper visual quadrant that is not part of DM. In addition, another visual area, M, is likely located at the DM tip of V3d. There is no evidence for a similar disruption of V3v. For the present, we favor continuing the traditional concept of V3 with the possible modification of a gap in V3d in at least some primates.