The visual system of birds includes an efferent projection from a visual area, the isthmo-optic nucleus in the midbrain, back to the retina. Using a combination of anterograde labeling of efferent fibers, reconstruction of dye-filled neurons, NADPH-diaphorase staining, and transmission electron microscopy, we have examined the distribution of efferent fibers and their synaptic structures in the chicken retina. We show that efferent fibers terminate strictly within the ventral retina. In two completely mapped retinas, only 2 fibers from a total of 15,359 terminated in the dorsal retina. The major synapse made by each efferent fiber is with a single efferent target amacrine cell (TC). This synapse consists of 5–25 boutons of 2 μm diameter, each with multiple active zones, pressed into the TC soma or synapsing with a basketwork of rudimentary TC dendrites in the inner nuclear layer (INL). This basketwork, which is sheathed by Muller cell processes, defines a private neuropil in the INL within which TCs were also seen to receive input from retinal neurons. In addition to the major synapse, efferent fibers typically produce several very thin processes that terminate nearby in single small boutons and for which the soma of a local amacrine cell is one of the likely postsynaptic partners. A minority of efferent fibers also give rise to a thicker process, terminating in a strongly diaphorase-positive ball about 5 μm in diameter.

We investigated the synaptic connectivity of two populations of recoverin-labeled bipolar cells and GABAergic neurons in the inner plexiform layer (IPL) of the rat retina. Two types of cone bipolar cells, type 2 and type 8, were stained with anti-recoverin antibodies, and GABAergic neurons were stained with anti-glutamic acid decarboxylase (GAD) antibodies. Type 2 cone bipolar axons received synaptic input from amacrine cell processes in 177 cases; among these amacrine cell processes, 92 processes (52.0%) were GAD-like immunoreactive. A total of 159 amacrine cell processes, which are presynaptic to type 8 cone bipolar cells, were observed. Among these processes, 117 processes (73.6%) were GAD-like immunoreactive. The postsynaptic elements at the ribbon synapses of recoverin-labeled cone bipolar cells were observed in 482 processes. In both type 2 and type 8 cone bipolar cells, the major output was to amacrine cell processes. At the ribbon synapses of the type 2 cone bipolar cells, 224 of the postsynaptic profiles were amacrine cell processes, 97 processes (43.3%) were GAD-like immunoreactive. In type 8 cone bipolar cells, 45 processes (30.2%) of 149 amacrine cell processes were GAD-like immunoreactive. Our results provide morphological evidence that GABA is a major transmitter involved in the visual processing of type 2 and 8 cone bipolar cells and GABA may have a stronger influence on type 8 cone bipolar cells than type 2 cone bipolar cells in the IPL of the rat retina.

Recently, we showed that contrast sensitivity for color and high–spatial frequency luminance stimuli is enhanced during smooth pursuit eye movements (Schütz et al., 2008). In this study, we investigated the enhancement over a wide range of temporal and spatial frequencies. In Experiment 1, we measured the temporal impulse response function (TIRF) for colored stimuli. The TIRF for pursuit and fixation differed mostly with respect to the gain but not with respect to the natural temporal frequency. Hence, the sensitivity enhancement seems to be rather independent of the temporal frequency of the stimuli. In Experiment 2, we measured the spatial contrast sensitivity function for luminance-defined Gabor patches with spatial frequencies ranging from 0.2 to 7 cpd. We found a sensitivity improvement during pursuit for spatial frequencies above 2–3 cpd. Between 0.5 and 3 cpd, sensitivity was impaired by smooth pursuit eye movements, but no consistent difference was observed below 0.5 cpd. The results of both experiments are consistent with an increased contrast gain of the parvocellular retinogeniculate pathway.

The PC pathway conveys both chromatic and achromatic information, with PC neurons being more responsive to chromatic (L−M) than to achromatic (L+M) stimuli. In considering the evolution of color vision, it has been suggested that the dynamic range of chromatic PC-pathway processing is tuned to the chromatic content of the natural environment. Anomalous trichromats, with reduced separation of their L- and M-cone spectral sensitivities, have diminished chromatic input to PC-pathway cells. Dichromats, with absent L or M cones, should have no chromatic input to PC-pathway cells. Therefore, the PC-pathway dynamic range of color defectives should be released from any constraint imposed by the chromatic environment. Here we ask whether this results in compensatory enhancement of achromatic PC-pathway processing in color defectives. This study employed a psychophysical method designed to isolate PC-pathway processing using achromatic stimuli. In a pulsed-pedestal condition, a four-square stimulus array appeared within a uniform surround. During a trial, one of the test squares differed from the other three, and the observer's task was to choose the square that was different. A four-alternative, forced-choice method was used to determine thresholds as a function of the contrast of the four-square array to the surround. Seven color defective and four normal observers participated. Results showed no systematic differences between normals and color defectives. There was no enhancement of achromatic processing as compensation for reduced chromatic processing in the PC-pathway system in color defectives. From physiological recordings, PC-pathway achromatic contrast gains of dichromatic and trichromatic New World primates and trichromatic Old World macaques have also been shown to be similar to each other. Our study and the animal studies imply that PC-pathway contrast gain parameters were regulated by factors other than the environmental chromaticity gamut, and may have arisen in a nontrichromatic common ancestor to both Old and New World primates.

We measured the photopic spectral sensitivity of multiunit activity in the torus longitudinalis and optic tectum of goldfish. Since negative contrast stimuli are most effective for exciting torus longitudinalis, spiking activity was evoked by the shadow of a disc moving through a monochromatic light beam projected upon a screen. The amount of activity evoked in torus longitudinalis generally increased with the monochromatic stimulus radiance at the same rate for all wavelengths, indicating a univariant response. Spiking activity in tectum, however, increased at different rates across the spectrum, indicating color-dependent responses. The action spectra for torus longitudinalis were all similar and relatively flat as expected of a homogeneous, broad-band luminance processing system, and about 1 log unit more sensitive than the tectal action spectra. The latter generally displayed sharp peaks and dips in sensitivity indicative of opponent processing.

We studied the visuomotor properties of 54 corticostriatal (CS) and 38 corticotectal (CT) neurons in a region of area 6 that largely corresponds to the cat's frontal eye fields in five cats trained to do simple oculomotor tasks. Overall, these cells were similar to the general population of area 6 neurons described in the previous paper (Weyand & Gafka, 1998), with very few showing pre-saccadic activity. Likewise, CS and CT cells were similar to each other, although only CS cells showed activity exclusively related to the delivery of the reward and CT cells were more likely to be active during saccades. Variability in visual response latencies and the observation that some cells showed initial visual suppression suggest CS and CT cells reflect the output of a variety of intracortical circuits. Despite similar response properties and overlapping laminar origin, CS and CT circuits appear largely independent. Among 32 cells that we could electrically activate (either synaptically or antidromically) from the superior colliculus, only two could also be activated from stimulating electrodes in the striatum. Similarly, 23 of 25 cells electrically activated from the striatum could not be activated from the superior colliculus. Although few of these efferent cells exhibited pre-motor activity, many exhibit properties that could contribute to gaze control.

It has been argued that in order for the visual system to detect edges accurately under a range of conditions, the visual system needs to adapt to the local contrast level to preserve sensitivity (Blakemore & Campbell, 1969). Cells in the primary visual cortex of cats adapt to stimuli with low to moderate contrast. Curiously, macaque monkey neurons in primary visual cortex (V1) do not show evidence for similar adaptation. To address the question of whether this differential sensitivity in contrast adaptation might be due to phylogenetic variation between cats and primates or to specializations for visual niche (e.g. nocturnal vs. diurnal), contrast adaptation to temporally and spatially optimized gratings was examined in 30 V1 cells of three nocturnal primate bush babies (Galago crassicaudatus). A second objective was to examine the relationship between the degree of contrast adaptation and cell classification or cell location relative to cortical layers or compartments [i.e. cytochrome-oxidase (CO) blobs and interblobs]. All cells were classified (simple vs. complex) and anatomically localized relative to cortical layers and cytochrome-oxidase (CO) blob and interblob compartments. Two independent measures of contrast adaptation were used. In the first test, contrast was sequentially increased from 3–56% and then decreased. The contrast required to maintain a half-maximum response amplitude in the 30 cells tested increased an average of 0.24 (±0.12) log units during the sequential decrements in contrast. For the second test, four sets of five interleaved contrasts within ±1 octave of a central adapting contrast (10%, 14%, 20%, and 28%, respectively) were presented. The cells produced a mean adaptation index of 0.57 (±0.47) which is very similar to that exhibited by cat cortical neurons (0.54 ± 0.41). Interestingly, cells in interblobs showed a trend toward greater adaptation than did blob cells. Moreover, cells in the supragranular layers exhibited greater adaptation than cells in the infragranular layers. No significant differences in adaptation were found to correlate with other cell classification indices. Taken together, our results suggest that contrast adaptation may be more important for maintaining sensitivity in nocturnal species (primates or cats) than in diurnal species (macaque monkeys), and that in the nocturnal bush baby, cells in cortical layers and compartments may be differentially specialized for contrast adaptation.

Dopaminergic interplexiform cells in the retina of the blue acara were investigated using an antiserum against tyrosine hydroxylase and PAP visualization. In whole-mount preparations, we observed a homogeneous distribution of cell bodies throughout the retina without any indication of regional specialization. At the fine and ultrastructural level, we studied the morphology of labeled telodendria within the outer plexiform layer. Apart from contacts with horizontal cell perikarya and bipolar cell dendrites, we observed direct contacts, mostly in the form of close appositions, with cone pedicles and rod spherules. Quantitative evaluation and reconstruction of serial sections showed that all cone pedicles and most rod terminals were approached in this way. The dopaminergic pathway terminating on horizontal cells and photoreceptors is discussed with respect to the localization of dopamine receptors in the outer retina, and the control of adaptive changes such as retinomotor movements, spinule formation, and horizontal cell coupling.

We have examined the retinal decussation patterns in pigmented ferrets that were either wild-type sable or heterozygous with one albino gene. Unilateral injections of horseradish peroxidase were made into the optic tract and labeled ganglion cells visualized in retinal wholemounts. In both wild-type and heterozygous ferrets, those ganglion cells in the temporal retina with the largest cell bodies projected only to the contralateral side of the brain. The total number of ipsilaterally projecting ganglion cells did not differ with the genotype of the animal. The numbers ranged from 5471–6759 cells. Unlike the cat, there is no difference in retinal decussation patterns in wild-type sable ferrets and heterozygous ferrets carrying one albino gene.

The number of subregions in the activity profiles of simple cells varies in different cells from 2–8; that is, the number of cycles in the weighting function varies from 1–4. The distribution of receptive-field (RF) sizes at eccentricities of 0-6 deg are clustered at half-octave intervals and form a discrete distribution with maxima at 0.62, 0.9, 1.24, 1.8, 2.48, and 3.4 deg. The spatial frequencies to which the cells are tuned are also clustered at half-octave intervals, forming a discrete distribution peaking at 0.45, 0.69, 0.9, 1.35, 1.88, 2.7, 3.8, and 5.6 cycles/deg. If we divide the RF sizes by the size of the period of the subregions, then the average indices of complexity (really existing) or the number of cycles in the weighting function form (after normalization) the sequences: 1, 1.41, 2.0, 2.9, 4.15.

The relation between the bandwidth of the spatial-frequency characteristic and the optimal spatial frequency is in accordance with predictions of the Fourier hypothesis. The absolute bandwidth does not change with the number of cycles/module. This means that inside the module the absolute bandwidth does not change with the number of the harmonic. The results allow us to suggest the following. A module of the striate cortex, which is a group of cells with RFs of equal size projected onto the same area of central visual field, accounts for the Fourier description of the image. The basis functions of the module are composed of four harmonics only, irrespective of size and position of the module.

Besides linear cells (sinusoidal and cosinusoidal elements), the module contains nonlinear cells, performing a nonlinear summation of the responses of sinusoidal and cosinusoidal elements. Such cells are characterized by an index of complexity which is more than the number of cycles in the weighting function and by marked overlap of ON and OFF zones. The analysis of organization suggests that the cells can measure the amplitude and phase of the stimulus.

Previous psychophysical evidence suggests that motion and orientation processing systems interact asymmetrically in the human visual system, with orientation information having a stronger influence on the perceived motion direction than vice versa. To investigate the mechanisms underlying this motion-form interaction we used moving and oriented Glass patterns (GPs), which consist of randomly distributed dot pairs (dipoles) that induce the percept of an oriented texture. In Experiment 1 we varied the angle between dipole orientation and motion direction (conflict angle). In separate sessions participants either judged the orientation or motion direction of the GP. In addition, the spatiotemporal characteristics of dipole motion were manipulated as a way to limit (Experiment 1) or favor (Experiment 2) the availability of orientation signals from motion (motion streaks). The results of Experiment 1 showed that apparent GP motion direction is attracted toward dipole orientation, and apparent GP orientation is repulsed from GP motion. The results of Experiment 2 showed stronger repulsion effects when judging the GP orientation, but stronger motion streaks from the GP motion can dominate over the signals provided by conflicting dipole orientation. These results are consistent with the proposal that two separate mechanisms contribute to our perception of stimuli which contain conflicting orientation and motion information: (i) perceived GP motion is mediated by spatial motion-direction sensors, in which signals from motion sensors are combined with excitatory input from orientation-tuned sensors tuned to orientations parallel to the axis of GP motion, (ii) perceived GP orientation is mediated by orientation-tuned sensors which mutually inhibit each other. The two mechanisms are revealed by the different effects of conflict angle and dipole lifetime on perceived orientation and motion direction.

The effects of kainate receptor-preferring glutamate ligands were tested on the electroretinogram (ERG) of the Xenopus retina. Kainate, domoic acid, and 5-iodowillardiine (20–100 μM) acted similarly in every respect. They increased peak amplitudes of the ERG a-, b-, and d-waves significantly over controls. The AMPA-specific antagonist, GYKI 53655, prevented a kainate-induced increase in ERG a- and d-waves, but was without effect on an increase in the b-wave. Once the effect of agonist on the b-wave had peaked, the ERG began to subside, leading to its nearly complete disappearance within 20 min. Prior exposure to GYKI followed by a combination of GYKI + agonist did not significantly slow the rate of b-wave disappearance. Our results indicate that (1) AMPA receptors contribute to ERG a- and d-waves. (2) The kainate-evoked increase in ERG a-, b-, and d-waves probably results, in part, from an excitotoxic swelling of inner retinal processes. (3) The inner retina has a population of GYKI-resistant, kainate-sensitive receptors which may contribute to b-wave generation.

Relational color constancy refers to the constancy of the perceived relations between the colors of surfaces of a scene under changes in the spectral composition of the illuminant. Spatial ratios of cone excitations provide a natural physical basis for this constancy, as, on average, they are almost invariant under illuminant changes for large collections of natural surfaces and illuminants. The aim of the present work was to determine, computationally, for specific surfaces and illuminants, the constancy limits obtained by the application of a minimum-variance principle to cone-excitation ratios and to investigate its validity in predicting observers' surface-color judgments. Cone excitations and their changes due to variations in the color of the illuminant were estimated for colored surfaces in simulated two-dimensional scenes of colored papers and real three-dimensional scenes of solid colored objects. For various test surfaces, scenes, and illuminants, the estimated levels of relational color constancy mediated by cone-excitation ratios varied significantly with the test surface and only with certain desaturated surfaces corresponded to ideal matches. Observers' experimental matches were compared with predictions expressed in CIE 1976 (u′,v′) space and were found to be generally consistent with minimum-variance predictions.

We have examined the distribution of metabotropic glutamate receptors (mGluRs) 1 and 5 in the adult chicken retina using preembedding immuno-electronmicroscopy. Immunoreactivity for mGluRs 1 and 5 was found in both the outer plexiform layer (OPL) and the inner plexiform layer (IPL). For mGluR1, OPL labeling was observed at cone pedicles and horizontal and bipolar cell processes. In the IPL, mGluR1 labeling could be found on bipolar cell terminals, as well as postsynaptic processes, including amacrine cell processes. Neither presynaptic nor postsynaptic elements were labeled at rod synapses. For mGluR5, OPL labeling was associated with cone pedicles as well as bipolar and horizontal cell processes. As for mGluR1, rod synapses were unlabeled. In the IPL, labeling for mGluR5 was found on bipolar cell terminals and amacrine cell processes. The presynaptic expression of these receptors in the OPL was confirmed at the light level by double-labeling experiments with SV2. The distributions of mGluRs 1 and 5 indicate that they have the potential to regulate function in both synaptic layers. Furthermore, the similar expression patterns for these two receptors indicate that they might be co-expressed and thus have the potential to interact functionally.

Action potentials in amacrine cells are important for lateral propagation of signals across the inner retina, but it is unclear how many subclasses of amacrine cells contain voltage-gated sodium channels or can fire action potentials. This study investigated the ability of amacrine cells with narrow (< 200 μm) and wide (> 200 μm) dendritic fields to fire action potentials in response to depolarizing current injections and light stimulation. The pattern of action potentials evoked by current injections revealed two distinct classes of amacrine cells; those that responded with a single action potential (single-spiking cells) and those that responded with repetitive action potentials (repetitive-spiking cells). Repetitive-spiking cells differed from single-spiking cells in several regards: Repetitive-spiking cells were more often wide field cells, while single-spiking cells were more often narrow field cells. Repetitive-spiking cells had larger action potential amplitudes, larger peak voltage-gated NaV currents lower action potential thresholds, and needed less current to induce action potentials. However, there was no difference in the input resistance, holding current or time constant of these two classes of cells. The intrinsic capacity to fire action potentials was mirrored in responses to light stimulation; single-spiking amacrine cells infrequently fired action potentials to light steps, while repetitive-spiking amacrine cells frequently fired numerous action potentials. These results indicate that there are two physiologically distinct classes of amacrine cells based on the intrinsic capacity to fire action potentials.

We examined the functional properties of a low-voltage-activated (LVA) calcium current in ganglion cells of the neotenous tiger salamander (Ambystoma tigrinum) retina. Our analysis was based on whole-cell recordings from acutely dissociated ganglion cell bodies identified by retrograde dye injections. Using a continuously perfused cell preparation, the LVA current was isolated with the use of potassium channel blocking agents added to the bathing medium and the pipette solution, while tetrodotoxin was added to the bathing medium to block Na+ channels. Approximately 70% of ganglion cells had an easily identified LVA current. The LVA current activated at membrane potentials more positive than −90 mV, and inactivated rapidly. It was relatively insensitive to nickel (IC50 > 500 μM) and amiloride (IC50 > 750 μM). Voltage- and current-clamp studies allowed us to generate a model of this current using the NEURON simulation program. Studies were also carried out to measure the LVA Ca2+ current in ganglion cells with dendrites to confirm that it had a significant dendritic representation. Physiological mechanisms that may depend on LVA Ca2+ currents are discussed with an emphasis on the role that dendrites play in ganglion cell function.

Sensory representations in the brain exhibit topographic variations in magnification. These variations have been thought to reflect regional differences in the density of innervation at the sensory receptor surface. In the primate visual cortex, for example, local magnification factors have been reported to be proportional to the corresponding densities of retinal ganglion cells. We sought to learn whether this principle also operates in a second major retinofugal pathway—the projection to the superior colliculus. In cats, we first used retrograde transport to determine the retinal distributions of the ganglion cells that project to the colliculus. Then, we compared the numbers of colliculopetal ganglion cells in selected retinal sectors to the areas of the corresponding collicular representations. Collicular areal magnification was not simply proportional to the density of afferent ganglion cells, being instead at least 5-fold greater than expected in the representation of the central visual field. These data imply that incoming retinal afferents are more widely spaced in the central regions of the tectal map than in the map's periphery. Such variations in afferent density appear to play as large a role as the distribution of ganglion cells in determining the metric of the collicular map.

Individuals are constantly bombarded by sensory stimuli across multiple modalities that must be integrated efficiently. Multisensory integration (MSI) is said to be governed by stimulus properties including space, time, and magnitude. While there is a paucity of research detailing MSI in aging, we have demonstrated that older adults reveal the greatest reaction time (RT) benefit when presented with simultaneous visual-somatosensory (VS) stimuli. To our knowledge, the differential RT benefit of visual and somatosensory stimuli presented within and across spatial hemifields has not been investigated in aging. Eighteen older adults (Mean = 74 years; 11 female), who were determined to be non-demented and without medical or psychiatric conditions that may affect their performance, participated in this study. Participants received eight randomly presented stimulus conditions (four unisensory and four multisensory) and were instructed to make speeded foot-pedal responses as soon as they detected any stimulation, regardless of stimulus type and location of unisensory inputs. Results from a linear mixed effect model, adjusted for speed of processing and other covariates, revealed that RTs to all multisensory pairings were significantly faster than those elicited to averaged constituent unisensory conditions (p < 0.01). Similarly, race model violation did not differ based on unisensory spatial location (p = 0.41). In summary, older adults demonstrate significant VS multisensory RT effects to stimuli both within and across spatial hemifields.

Endothelin-1 (ET-1), a potent vasoconstrictor peptide, has been implicated in the development of normal- and high-tension glaucoma. We investigated the effects of unoprostone on extracellular signal-regulated kinase (ERK) in ET-1-induced retinal ganglion cell (RGC) death and optic nerve injury. Our morphometric study showed that intravitreal injection of ET-1 led to cell loss in the RGC layer (RGCL) in 28 days. Western blot analysis showed decreased neurofilament (NF) protein in the optic nerve 28 days after ET-1 injection. In this in vivo model, increased phosphorylated ERK (p-ERK) was observed in the retina on 1 day and subsequently in the optic nerve from 7 days after ET-1 injection. Simultaneous injection of M1, as a metabolite of unoprostone, showed further increased p-ERK levels compared with ET-1 injection alone. Our morphometric study of flat-mount preparations stained with cresyl violet or retrograde labeling with a neuro-tracer and Western blot analysis of NF showed that inhibition of ERK phosphorylation led to acceleration of ET-1-induced RGC death and optic nerve damage. In addition, M1 significantly attenuated both RGC loss and the decrease in NF protein induced by ET-1. The protective effects of M1 were significantly inhibited by U0126, an ERK inhibitor. These results suggest that unoprostone has neuroprotective effects against ET-1-induced neuronal injury through ERK phosphorylation.

The survival and function of retinal neurons is dependent on mitochondrial energy generation and its intracellular distribution by creatine kinase. Post ischemic disruption of retinal creatine synthesis, creatine kinase activity, or transport of creatine into neurons may impair retinal function. S-adenosyl-l-methionine (SAMe) is required for creatine synthesis, phosphatidylcholine and glutathione synthesis, and transducin methylation. These reactions are essential for photoreceptor function but may be downregulated after ischemia due to a reduction in SAMe. Our aim was to determine whether administration of SAMe after ischemia could improve retinal function. Unilateral retinal ischemia was induced in adult rats by increasing the intraocular pressure to 110 mm Hg for 60 min. Immediately after the ischemic insult, SAMe was injected into the vitreous (100 μm), followed by oral administration (69 mg/kg/day) for 5 or 10 days. Retinal function (electroretinography), histology, and creatine transporter (CRT-1) expression were analyzed. Photoreceptoral responses (RmP3, S), rod and cone bipolar cell responses (PII), and oscillatory potentials were reduced by the ischemia/reperfusion insult. Although SAMe treatment ameliorated the ischemia-induced histological damage by day 5, there was no improvement in retinal function and the intensity of CRT-1 labeling in ischemic retinas was markedly reduced. However, 10 days after ischemia, a recovery in CRT-1 immunolabeling was evident and SAMe supplementation significantly restored photoreceptor function and rod PII responses. In conclusion, these data suggest that creatine transport and methylation reactions, such as creatine synthesis, may be compromised by an ischemic insult contributing to retinal dysfunction and injury. Oral SAMe supplementation after retinal ischemia may provide an effective, safe, and accessible neuroprotective strategy.