The distribution of cytochrome oxidase (CO) in the lateral geniculate nucleus (LGN) of normal adult macaque monkeys was analyzed in quantitative light- and electron-microscope (EM) studies. Both reactive and nonreactive neurons were found throughout laminae 1–6. Darkly reactive neurons were more numerous in laminae 1, 2, and 6. Within each lamina, there was a positive correlation between cell size and level of CO activity in neurons. The cell density was greater in laminae 1, 4, and 6, which received input from the contralateral eye, than in corresponding laminae representing the ipsilateral eye (2, 3, and 5). The cell density in each of the magnocellular laminae was less than that in each of the parvicellular laminae.

Three types of neurons could be distinguished within magnocellular laminae at the EM level. Types I and II were interpreted to be relay neurons, while the small size of type III qualified them to be interneurons. Two populations were found within parvicellular laminae, corresponding to relay neurons and interneurons, respectively. EM quantitative analyses revealed that the darkly reactive neurons contained a high proportion of moderate to darkly reactive mitochondria, which comprised 44.2%, 42.5%, and 39.2% of the mitochondrial population within neurons of laminae 1, 2, and 6 respectively. In contrast, a relatively low proportion of reactive mitochondria were found in neurons within laminae 3 (22.8%), 4 (26.4%), and 5 (32.4%). Moreover, magnocellular laminae contained a higher density of synapses on cell bodies than parvicellular laminae. All laminae, except layer 5, contained predominantly symmetric synapses on cell bodies. However, the proportion of symmetrical synapses in the magnocellular laminae (65.6%) was greater than that in the parvicellular laminae (59%).

Our quantitative light and EM results indicate that the level of metabolic activity in neurons of the monkey LGN is higher in magnocellular, ON-center, and contralateral than in parvicellular, OFF-center, and ipsilateral visual pathways, respectively. The metabolic activity of neurons is likely to reflect the chronic level of spontaneous and synaptically evoked discharges of these cells.

This paper presents a modified reciprocal inhibition model for the temporal dynamics of binocular rivalry. The model is based on neurophysiological mechanisms and is derived from human psychophysical data. A simple reciprocal inhibition oscillator may be described with a set of four coupled differential equations with a neurophysiological interpretation. However, such a circuit does not account for some aspects of the temporal behavior of binocular rivalry, including the effects of contrast change on alternation rate and on the magnitudes of changes in duration of the suppressed and dominant phases. To better account for these phenomena, the equations and their simulation are modified to include three new components: (1) presynaptic inhibition of the reciprocal inhibition by the input, (2) the motor delays that occur when a human observer tracks rivalry and (3) a minimum threshold for each neuron's state variable. The result is a much improved fit to psychophysically-obtained data on the temporal behavior of binocular rivalry. Finally, the model is incorporated into a larger model to suggest how rivalry might occur in a network that usually exhibits binocular fusion.

The responses of monkey retinal ganglion cells to sinusoidal stimuli of various temporal frequencies were measured and analyzed at a number of mean light levels. Temporal modulation tuning functions (TMTFs) were measured at each mean level by varying the drift rate of a sine-wave grating of fixed spatial frequency and contrast. The changes seen in ganglion cell temporal responses with changes in adaptation state were similar to those observed in human subjects and in turtle horizontal cells and cones tested with sinusoidally flickering stimuli; “Weber's Law” behavior was seen at low temporal frequencies but not at higher temporal frequencies. Temporal responses were analyzed in two ways: (1) at each light level, the TMTFs were fit by a model consisting of a cascade of low- and high-pass filters; (2) the family of TMTFs collected over a range of light levels for a given cell was fit by a linear negative feedback model in which the gain of the feedback was proportional to the mean light level. Analysis (1) revealed that the temporal responses of one class of monkey ganglion cells (M cells) were more phasic at both photopic and mesopic light levels than the responses of P ganglion cells. In analysis (2), the linear negative feedback model accounted reasonably well for changes in gain and dynamics seen in three P cells and one M cell. From the feedback model, it was possible to estimate the light level at which the dark-adapted gain of the cone pathways in the primate retina fell by a factor of two. This value was two to three orders of magnitude lower than the value estimated from recordings of isolated monkey cones. Thus, while a model which includes a single stage of negative feedback can account for the changes in gain and dynamics associated with light adaptation in the photopic and mesopic ranges of vision, the underlying physical mechanisms are unknown and may involve elements in the primate retina other than the cone.

Saccades evoked electrically from the deep layers of the superior colliculus have been examined in the alert cat with its head fixed. Amplitudes of the vertical and horizontal components varied linearly with the starting position of the eye. The slopes of the linear-regression lines provided an estimate of the sensitivity of these components to initial eye position. In observations on 29 sites in nine cats, the vertical and horizontal components of saccades evoked from a given site were rarely influenced to the same degree by initial eye position. For most sites, the horizontal component was more sensitive than the vertical component. Sensitivities of vertical and horizontal components were lowest near the representations of the horizontal and vertical meridians, respectively, of the collicular retinotopic map, but otherwise exhibited no systematic retinotopic dependence. Estimates of component amplitudes for saccades evoked from the center of the oculomotor range also diverged significantly from those predicted from the retinotopic map. The results of this and previous studies indicate that electrical stimulation of the cat's superior colliculus cannot yield a unique oculomotor map or one that is in register everywhere with the sensory retinotopic map. Several features of these observations suggest that electrical stimulation of the colliculus produces faulty activation of a saccadic control system that computes target position with respect to the head and that small and large saccades are controlled differently.

Desensitization of cGMP-activated channels was examined in excised, inside-out patches obtained from rod photoreceptors. Cyclic GMP was applied using a rapid-flow system in which concentration jumps are complete within 10–50 ms. In outer-segment patches containing many channels, the cGMP-dependent conductance reached a steady plateau that was maintained for tens of seconds in the presence of cGMP; thus, there was no indication of slow desensitization. However, rapid desensitization on the scale of milliseconds could not be ruled out because of limited speed of access of cGMP to the inner face of the patch membrane. To test for rapid desensitization, inner-segment patches containing only a single cGMP-activated channel were used. In these one-channel patches, there was no change in activity of the channel with time from its earliest onset after application of cGMP, indicating that rapid desensitization also did not occur.

In albinos, the retinofugal projections to the ipsilateral side of the brain are reduced (e.g., see Guillery, 1969; LaVail et al., 1978; Lund, 1965). Although all ganglion cell types are affected, in mice the displaced ganglion cell population is the main target of the albino mutation (Dräger & Olsen, 1980). Here we tested whether this preferential effect on displaced ganglion cells is a general consequence of the melanin reduction or a pleiotropic effect unique to the albino locus, retrogradely tracing tracing retinal ganglion cells in normal C57BL/6J mice and in several non-allelic hypopigmentation mutants on the same background: albino (C57BL/6J-c2J), beige (C57BL/6J-bg), pale ear (C57BL/6J-ep), ruby-eye/haze (C57BL/6J-ru-2hz), and pearl (C57BL/6J-pe). All mutants have lower overall cell counts in the ipsilateral projection, but the displaced population is disproportionately affected: the albinos contain 42% of the normal number of displaced ganglion cells, and the other mutants have an average 57% of normal counts.

The reduction in uncrossed retinofugal projections in albinos affects the inputs to the lateral geniculate nucleus and the superior colliculus, but not to the suprachiasmatic nucleus (Dräger, 1974). To address the question in which way the susceptible uncrossed projections differ from the nonsusceptible one, we compared ganglion cells backfilled from the suprachiasmatic nucleus to ganglion cells backfilled from the optic tract at geniculate level. Whereas the uncrossed optic tract projection originates from the binocular region in the ventro-temporal retina and contains a high fraction of large and displaced ganglion cells (Dräger & Olsen, 1980), both the crossed and uncrossed inputs to the suprachiasmatic nucleus originate from the entire retina with a relative preference for the lower nasal region that corresponds to part of the monocular visual field; all ganglion cells projecting to the suprachiasmatic nucleus are of medium size, and they are located in the ganglion cell layer.

These observations allow the following conclusions: (1) All genetic mutants which cause a reduction in ocular melanin, regardless of the molecular or cell-biological mechanism underlying the pigment reduction, result in decreased uncrossed projections; this confirms previous reports (LaVail et al., 1978, Sanderson et al., 1974). (2) The decrease affects only projections involved in binocular vision. (3) In mice, the ganglion cells displaced to the inner nuclear layer, and hence located closer to the retinal pigment epithelium, are disproportionately affected by the melanin reductions. These observations may provide cues to the spatio-temporal mechanism of the melanin action in the embryonic visual system.

In the rods of Bufo marinus and other species, bleaching of the rhodopsin in isolated cells leads to a loss of sensitivity and response amplitude and to a shortened response duration. These changes are permanent for cells bathed in Ringer&s solution. They are due to as yet unknown modulations in the transduction biochemistry. In this paper, we report that these changes can be partly or completely reversed by supplying biotin, pyruvate, and elevated glucose to the rod. The time course of this reversal and the substances which promote it imply that these are metabolically mediated effects. Based on the reported action of biotin and pyruvate on the one hand and on the changes of the response waveforms on the other hand, we believe that the phenomena we observe involve the later steps of the transduction cycle.

Photoreceptors periodically shed light-sensitive membranes; rods at light onset, cones at night. The spectral characteristics of light required to initiate shedding by 502-rods were studied in the frog retina. After 24 h of white light, animals were dark primed for 1 h then presented with 1 h of nearly monochromatic light to induce the shedding response. The light delivered a total photon flux of 2.5 or 0.5 μE/m2s. Following conventional fixation and plastic embedding, 1 μm sections were examined with light microscopy. The number of photoreceptor tips (phagosomes) shed by 100 consecutive rods were counted and plotted as a function of wavelength. Bright light induced at least 15 phagosomes per 100 rods at all wavelengths tested, 420−640 nm, and this shedding was more than doubled with light from 540−600 nm. When the light was dimmed, there was no shedding response except for this 540−600 nm window. This shedding peak closely corresponds to the absorbance curve of the frog's 575-cone photopigment and implies that the 575-cone can drive rod shedding. The broad background effect further indicates that all photoreceptors have an input and suggests that a luminosity cell, such as the internal horizontal cell, may be involved.

The glycinergic system in goldfish retina was studied by immunocytochemical localization of glycine antiserum at the light-microscopical level. Numerous amacrine cells, a type of interplexiform cell, interstitial cell, and displaced amacrine cell were glycine-immunoreactive (IR). Amacrine cells, accounting for 97% of the glycine-IR neurons, were of four types based solely on their level of dendritic stratification: stratified amacrine cells of the first, third, and fifth sublayers and bistratified amacrine cells of the first and fifth sublayers. Double-labeling experiments were carried out to determine possible co-localization of glycine-IR with GABA-IR, serotonin-IR, substance P-IR and somatostatin-IR. No evidence for co-localization of glycine-IR with these other transmitter substances was found, despite reports of co-localization of these substances in retinas of other species. Glycinergic neurons in goldfish retina appear to consist of a heterogeneous population of at least seven morphologically distinct subtypes that are also neurochemically distinct in regard to GABA, serotonin, substance P, and somatostatin. Since dendritic stratification in the inner plexiform layer is correlated with ON-, OFF-response types, we suggest that the subtypes of glycine-IR amacrine cells play different roles in the encoding of visual information.

Extracellular recordings from single units in the dorsal terminal nucleus (DTN) of the cat accessory optic system (AOS) were before and after intravitreal injections of the GABA antagonist bicuculline methiodide (BMI). Direction-selective responses of DTN cells elicited through the contralateral, injected eye were aboloshed 7−12 h following the injection. For the concentrations tested, direction-selective responses through the contralateral (injected) eye did not recover within 26 h. Direction-selective responses through stimulation of the ipsilateral (uninjected) eye were also dramatically depressed for 1−9 h after contralateral eye injections. However, direction-selective responses through the ipsilateral eye eventually returned and were often more vigorous in the final stages. BMI injections into the ipsilateral eye failed to block direction-selective responses through the ipsilateral eye. The effects of intravitreal BMI on contralateral eye responses imply that DTN units receive input from direction-selective retinal ganglion cells. In addition, these results suggest that direction-selective input to the DTN from the visual cortex is independent of the retinal pathway. Using pharmacological methods described here, for the first time direction-selective responses of AOS units driven through the ipsilateral eye can be experimentally isolated.

We have examined the morphology and distribution of neurones that contain nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase in human retinae. NADPH-diaphorase reactivity was observed in three different classes of amacrine cells (ND1, ND2, ND3 cells) and in the cone photoreceptors. ND1 cells had relatively large somata (mean, 12.3 ¼m) located in the inner nuclear layer (INL) and in the ganglion cell layer (GCL). Their dendrites were often strongly labeled and spread into either the middle or outer strata of the inner plexiform layer (IPL). The somata of ND2 cells were medium-sized (mean, 8.2 ¼m) and located in the INL and in the GCL; their dendrites were usually beaded and often spread in either the middle or outer strata of the IPL. ND3 cells had small, round somata (mean, 5.2 ¼m) located in either the INL or GCL, and were without labeled processes. The total number of NADPH-diaphorase cells (all classes) was estimated at 118,000, with a mean density of about 100/mm2. The most striking fea ture of NADPH-diaphorase cells in humans was that their distribution was relatively uniform across the retina, with no evidence of a peak in density at the foveal rim.

This commentary extends the review by Hiroyuki Uchiyama (1989) entitled “Centrifugal pathways to the retina: influence of the optic tectum” Visual Neuroscience 3, 183–206. A further scrutiny is made of the topography of the isthmo-retinal projection of the pigeon, which provides the most fully investigated example of a retinopetal projection. It is suggested that the topographical organization in this system is compatible with it's input being derived from the lower visual field (and upper retina) and it's output being directed to the horizon and lower retina. This is another form of attentional hypothesis for the centrifugal pathway, compatible with a role in ground feeding, and is testable by current tracing techniques in neurobiology.

When a cortical neuron receives synaptic input from both eyes, do the synaptic pathways that mediate the input from each eye match? In this study, inputs from the two eyes were compared by measuring the latencies of EPSPs and IPSPs evoked by electrical stimulation of the two optic nerves. For binocular neurons, these latencies invariably matched closely, indicating that the pathways from the two eyes contain the same number of synapses; monosynaptic input from lamina A of the lateral geniculate nucleus (LGN) is always matched by monosynaptic input from lamina A1. Conversely, polysynaptic input from one eye, either excitatory or inhibitory, is invariably accompanied by similar input from the other eye. In addition, the match between the two eyes in latency indicates that for each eye a synaptic potential is mediated by the same type of afferent, either X or Y.

Judging from intracellular recording, 75% of the neurons studied were binocular, that is, EPSPs could be evoked from either eye. In the remaining 25%, EPSPs could be evoked from only one eye, in agreement with extracellular receptive field studies in which 30% of cortical neurons are monocular.