We propose that there exists within the avian, and perhaps more generally in the vertebrate retina, a two-state nonadapting flip-flop circuit, based on reciprocal inhibitory interactions between the photoreceptors, releasing melatonin, the dopaminergic amacrine cells, and amacrine cells which contain enkephalin-, neurotensin-, and somatostatin-like immunoreactivity (the ENSL1 amacrine cells). This circuit consists of two loops, one based on the photoreceptors and dopaminergic amacrine cells, and the other on the dopaminergic and ENSLI amacrine cells. In the dark, the photoreceptors and ENSL1 amacrine cells are active, with the dopaminergic amacrine cells inactive. In the light, the dopaminergic amacrine cells are active, with the photoreceptors and ENSLI amacrine cells inactive. The transition from dark to light state occurs over a narrow (<1 log unit) range of low light intensities, and we postulate that this transition is driven by a graded, adapting pathway from photoreceptors, releasing glutamate, to ON-bipolar cells to dopaminergic amacrine cells. The properties of this pathway suggest that, once released from the reciprocal inhibitory controls of the dark state, dopamine release will show graded, adapting characteristics. Thus, we postulate that retinal function will be divided into two phases: a dopamine-independent phase at low light intensities, and a dopamine-dependent phase at higher light intensities. Dopamine-dependent functions may show two-state properties, or two-state properties on which are superimposed graded, adapting characteristics. Functions dependent upon melatonin, the enkephalins, neurotensin, and somatostatin may tend to show simpler two-state properties. We propose that the dark-light switch may have a role in a range of light-adaptive phenomena, in signalling night-day transitions to the suprachiasmatic nucleus and the pineal, and in the control of eye growth during development.

The purpose of the present study was to assess changes in the levels of cytochrome oxidase (CO) activity in the dorsal lateral geniculate nucleus (dLGN) of the adult cat following removal of primary visual cortical areas 17 and 18 on the day of birth (P1), P28, or in adulthood (≫6 months). Cytochrome oxidase activity was measured in histological sections 9 or more months after the cortical ablation. Control measures obtained from intact cats show that CO activity is normally highest in the A-laminae of dLGN, and slightly lower in the C-complex. Following visual cortex ablations incurred at any age, CO activity levels are reduced in the A-laminae. This reduction is most profound following ablations incurred on P28 or in adulthood. In contrast, CO activity in the C-complex of dLGN is at nearly normal levels following ablations on P1 or P28, but not in adulthood. These findings contribute to our understanding of the role played by the dLGN in the transfer of visual signals along retino-geniculo-extrastriate pathways that expand following early removal of areas 17 and 18. Moreover, they have implications for our understanding of spared behavioral functions attributed to the extrastriate cortex in cats which incurred early damage of areas 17 and 18.

Relay cells of the lateral geniculate nucleus, like those of other thalamic nuclei, manifest two distinct response modes, and these represent two very different forms of relay of information to cortex. When relatively hyperpolarized, these relay cells respond with a low threshold Ca2+ spike that triggers a brief burst of conventional action potentials. These cells switch to tonic mode when depolarized, since the low threshold Ca2+ spike, being voltage dependent, is inactivated at depolarized levels. In this mode they relay information with much more fidelity. This switch can occur under the influence of afferents from the visual cortex or parabrachial region of the brain stem. It has been previously suggested that the tonic mode is characteristic of the waking state while the burst mode signals an interruption of the geniculate relay during sleep. This review surveys the key properties of these two response modes and discusses the implications of new evidence that the burst mode may also occur in the waking animal.

Axon-bearing amacrine cells in mammalian retinae are encountered relatively infrequently during electrophysiological investigations, and thus very little is known about their physiological properties. Patch-clamp electrodes were used to record light responses from two axon-bearing amacrine cells in flat-mounted, dark-adapted rabbit retina. The recorded cells were stained, and the morphology visualized. Both cells were capable of generating action potentials. In one case, a linear relationship between mean depolarization and action-potential frequency was demonstrated. The cells had a proximal dendritic arbor and a morphologically distinct, much larger axon terminal system. The receptive field of the center response was coextensive with the dendritic arbor, and thus also much smaller than the axon terminal system. The center response was suppressed by activation of an inhibitory surround. Both cells responded to center illumination with an inward current which became more transient as the size of the illuminating spot was increased. It is suggested that axon-bearing amacrine cells receive input over a receptive field defined by the dendritic arbor, and distribute their output over a much more extensive axon terminal system, most probably via action potentials.

Photocurrents of cones in the retinas of a small fish, Danio aequipinnatus (Cyprinidae) were recorded with suction pipette electrodes. Spectral sensitivity was measured between 277 and 697 nm. Four spectral classes of cone were found, with λmax at 560, 480, 408, and 358 nm. For the latter, we provide the first complete characterization of spectral sensitivity of a vertebrate ultraviolet (UV) photoreceptor. All cones responded with similar kinetics, except for a subset of the 560-nm cones, which were distinctly faster. The a-bands of the three cones absorbing maximally in the visible have the same bandwidth when log sensitivity is plotted versus normalized frequency, and in this respect they are indistinguishable from primate cones (“Mansfield's rule’). An eighth-degree polynomial in λmax/λ based on this combined data set (fish, primate) is presented as a template that is likely to have predictive value in describing cone spectra from other vertebrates. The α−band of the UV cone, however, is somewhat narrower than predicted by this function, is similar to other UV visual pigments, and an eighth-degree polynomial that describes its shape is also presented. These measurements also provide information on the β−band (i.e. cis peak region), difficult to obtain by microspectrophotometry. The β−band of cone pigments is found at longer wavelengths as the α−band shifts toward the red. A secondary rise in cone sensitivity around 280 nm indicates that photons absorbed by aromatic amino acids in the opsin (γ−band) excite the transduction cascade, but the quantum efficiency is not as high as when absorption occurs in the retinal-protein chromophore.

Modes of storage and mechanisms of formation of 11-cis retinoids in the eyes of animals vary widely among the major phyla. We here describe evidence from two species of macruran decapod crustacea that point to different processes from those known in insects, the other group of arthropods for which there is extensive data. The eyes of the lobster (Homarus) contain about 300 pmol of retinal, somewhat less free retinol, and variable amounts (up to 1000+ pmol) of two retinyl esters, over 90% of which contain retinol in the 11-cis configuration. The major ester contains the long chain, polyunsaturated fatty acid docosahexaenoate (C22:6), but retinyl oleate (C18:1) is also present. Crayfish (Procambarus) contain the same retinyl esters, although in much smaller amounts. Homogenates of the eyes of both species are capable of isomerizing all-trans retinyl docosahexaenoate to the 11-cis configuration without using the energy of light. Crude fractionation of homogenates shows isomerase activity associated with membranes. The reaction mechanism has not been explored in detail, but on the basis of present evidence it may be similar to that found in vertebrate pigment epithelium. It is clearly different from the light-dependent processes known in insects (Hymenoptera and Diptera) and cephalopod mollusks, where isomerization takes place at the level of the aldehyde and 11-cis retinyl esters are not present as major storage reserves.

Adaptation of visual cortical cells' responses is observed following repeated presentation of grating stimuli. Grating adaptation is believed to exist only at the cortical level. The purpose of this study was to see if grating adaptation also occurs in the lateral geniculate nucleus. We studied the responses of 164 relay cells in layer A and A1 of the dorsal lateral geniculate nucleus (LGNd) to grating stimuli. Normal cats, as well as cats in which visual cortex was ablated, were studied. Adaptation was investigated using repeated presentation of gratings of different contrasts and orientations. The results showed the following: (1) Grating adaptation reduced the responses of 46% of the LGNd cells recorded. The responses normally decreased within 30 s and then stabilized. However, there was heterogeneity in the effects observed. About 38% of the cells studied were not affected by the adapting gratings. Some cells (16%) showed facilitation rather than habituation of their responses to test stimuli. (2) There was no significant difference between X and Y cells in their susceptibility to adaptation. This suggests that grating adaptation is a general property, independent of cell type. (3) The contrast-response curves of 57% of the LGNd cells studied shifted down after exposure to high-contrast adapting gratings. (4) Adapting gratings of the cells' preferred orientation decreased the orientation sensitivity of 56% of the orientation-sensitive cells. Adapting gratings at the nonpreferred orientation did not affect orientation sensitivity. (5) Prolonged grating adaptation also reduced the responses of 49% of the LGNd cells after inactivation of cortical inputs to the LGNd.

The distribution of neurons and fibers immunoreactive (ir) to the three calcium-binding proteins parvalbumin (PV), calbindin D-28k (CB), and calretinin (CR) was studied in the human lateral geniculate nucleus (LGN), lateral inferior pulvinar, and optic radiation, and related to that in the visual cortex. In the LGN, PV, CR, and CB immunoreactivity was present in all laminae, slightly stronger in the magnocellular than in the parvocellular laminae for CB and CR. PV-ir puncta, representing transversally cut axons, and CR-ir fibers were revealed within the laminae and interlaminar zones, and just beyond the outer border of lamina 6 in the geniculate capsule. In the optic radiation both PV- and CR-immunoreactive neurons, puncta, and fibers were present. CB immunoreactivity was revealed in neurons of all laminae of the lateral geniculate nucleus, including S lamina and interlaminar zones. There were hardly any CB-ir puncta or fibers in the laminae, interlaminar zones, geniculate capsule, or optic radiation. In the lateral inferior pulvinar, immunoreactive neurons for the three calcium-binding proteins were present in smaller number than in the LGN, as well as PV-ir puncta and CR-ir fibers within the nucleus and in the pulvinar capsule. In the white matter underlying area 17, fibers intermingled with a few scattered neurons were stained for both PV and CR, but very rarely for CB. These fibers stopped at the limit between areas 17 and 18. Area 17 showed a dense plexus of PV-ir puncta and neurons in the thalamo-receptive layer IV and CR-ir puncta and neurons both in the superficial layers I-II, IIIC, and in layer VA. Cajal-Retzius CR-ir neurons were present in layer I. CB-ir puncta were almost confined to layer I-III and CB-ir neurons to layer II. Finally the superior colliculus exhibited mostly populations of PV and CR pyramidal-like immunoreactive neurons, mainly in the intermediate tier. These data suggest that in the visual thalamus most calcium-binding protein immunoreactive neurons project to the visual cortex, while in the superior colliculus a smaller immunoreactive population represent projection neurons.

Various residual visual capacities have been reported for the phenomenally blind field of hemispherectomized patients, providing evidence for the relative roles of cortical and subcortical pathways in vision. We attempted to characterize these functions by examining the ability of five patients to detect, localize, and discriminate high-contrast flashed, flickering and moving targets. Dependent measures were verbal, manual, and oculomotor responses. As a control for light scatter, intensity thresholds for monocular detection of targets in the hemianopic field were compared with thresholds obtained when using an additional half eyepatch to occlude the blind hemiretina of the tested eye. One unilaterally destriate patient was tested on the same tasks. In photopic conditions, none of the hemispherectomized patients could respond to visual cues in their impaired fields, whereas the destriate patient could detect, discriminate, and point to targets, and appreciate the apparent motion of stimuli across his midline. Under reduced lighting, the threshold luminance required by hemispherectomized patients to detect stimuli presented monocularly was similar to that required for their detection when all visual information was occluded in the blind field, and only available to the visual system indirectly via light scatter. In contrast, the destriate patient's monocular threshold in his blind field was substantially lower than that for stimuli directly occluded in the blind field. As we found no range of stimuli which the hemispherectomized patients could detect or discriminate that was not also associated with discriminable scattered light, we conclude that the subcortical pathways which survive hemispherectomy cannot mediate voluntary behavioural responses to visual information in the hemianopic field.

Rod bipolar cells constitute the second-order neuron in the rod pathway. Previous investigations of the rabbit retina have evaluated the development of other components of the rod pathway, namely the dopaminergic and All amacrine cell populations. To gain further insights into the maturation of this retinal circuitry, we studied the development of rod bipolar cells, identified with antibodies directed to the α isoform of protein kinase C (PKC), in the rabbit retina. Lightly immunostained PKC-immunoreactive (IR) somata are first observed at postnatal day (PND) 6 in the distal inner nuclear layer (INL). Immunostaining is also observed in the outer plexiform layer (OPL), indicating the presence of PKC-IR dendrites. PKC-IR axons are present in the INL oriented toward the inner plexiform layer (IPL). Several of them terminate with enlarged structures resembling growth cones. At PND 8, some immunostained terminal bulbs, characteristic of rod bipolar cells, are detected in the proximal IPL. PKC-IR cells at PND 11 (eye opening) display stronger immunostaining and more mature characteristics than at earlier ages. The dendritic arborizations of these cells in the OPL and their axon terminals in the IPL attain mature morphology at later ages (PND 30 or older). The density of PKC-IR cells shows a peak at PND 11 followed by a drastic decrease up to adulthood. The total number of PKC-IR cells increases from PND 6 to PND 11 and then it remains almost unchanged until adulthood. The mosaic of PKC-IR cells is nonrandom in some retinal locations at PND 6, but the overall regularity index at PND 6 is lower than at older ages. The present data provide a comprehensive evaluation of the development of rod bipolar cells in the postnatal rabbit retina and are consistent with those previously reported for dopaminergic and All amacrine cell populations, indicating that different components of the rod pathway follow a similar pattern of maturation, presumably allowing the rod pathway to be functional at eye opening.

Although the neural location of the plaid motion coherence process is not precisely known, the middle temporal (MT) cortical area has been proposed as a likely candidate. This claim rests largely on the neurophysiological findings showing that in response to plaid stimuli, a subgroup of cells in area MT responds to the pattern direction, whereas cells in area V1 respond only to the directions of the component gratings. In Experiment 1, we report that the coherent motion of a plaid pattern can be completely abolished following adaptation to a grating which moves in the plaid direction and has the same spatial period as the plaid features (the so-called “blobs”). Interestingly, we find this phenomenon is monocular: monocular adaptation destroys plaid coherence in the exposed eye but leaves it unaffected in the other eye. Experiment 2 demonstrates that adaptation to a purely binocular (dichoptic) grating does not affect perceived plaid coherence. These data suggest several conclusions: (1) that the mechanism determining plaid coherence responds to the motion of plaid features, (2) that the coherence mechanism is monocular, and thus (3), that it is probably located at a relatively low level in the visual system and peripherally to the binocular mechanisms commonly presumed to underlie two-dimensional (2-D) motion perception. Experiment 3 examines the spatial tuning of the monocular coherence mechanism and our results suggest it is broadly tuned with a preference for lower spatial frequencies. In Experiment 4, we examine whether perceived plaid direction is determined by the motion of the grating components or the features. Our data strongly support a feature-based model.

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.

This study describes the connectivity between horizontal cells and short-wavelength-sensitive (SWS) cones in macaque monkey retina. H1 and H2 horizontal cells were either labelled with the carbocyanine dye, Dil, or injected intracellularly with Neurobiotin. The retinas were then processed with an antiserum against human SWS cone pigment, which usually stained the entire SWS cone. In these double-labelled retinas, the pattern of connectivity of H1 (n = 91) and H2 (n = 7) cells with SWS cones has been determined. About 85% of the H1 cells examined do not contact SWS cones. The dendritic terminal knobs of five H1 cells that do contact SWS cones were counted. They have, at most, 3% of their dendritic terminal knobs at SWS cones. All H2 cells examined make contact with SWS cones. The dendritic terminal knobs of one H2 cell were counted; about 11% of the dendritic terminal knobs are at the SWS cone. We conclude that horizontal cells in macaque monkey retina show specific patterns of connectivity to SWS cones.

We examined the effects of picrotoxin and pentylenetetrazol (PTZ) on the responses to motions of ON-OFF directionally selective (DS) ganglion cells of the turtle's retina. These drugs are antagonists of the inhibitory neurotransmitter GABA. For continuous motions, picrotoxin markedly reduced the overall directionality of the cells. In 21% of the cells, directional selectivity was lost regardless of speed and contrast. However, other cells maintained their preferred direction despite saturating concentrations of picrotoxin. And in most cells, loss, maintenance, or even reversal of preferred and null directions could occur as speed and contrast were modulated. In 50% of the cells, reversal of preferred and null directions occurred at some condition of visual stimuli. However, picrotoxin did not tend to alter the preferred-null axis for directional selectivity. For apparent motions, picrotoxin made motion facilitation, which normally occurs exclusively in preferred-direction responses, to become erratic and often occur during null-direction motions. Finally, PTZ had effects similar to picrotoxin but with less potency. The results in this paper indicated that models of directional selectivity based solely on a GABAergic implementation of Barlow and Levick's asymmetric-inhibition model do not apply to the turtle retina. Alternative models may comprise multiple directional mechanisms and/or a symmetric inhibitory one, but not asymmetric facilitation.

Male Cebus monkeys are all dichromats, but about two thirds of the females are trichromats. M and P retinal ganglion cells were studied in the male Cebus monkey to investigate the relationship of their morphology to retinal eccentricity. Retinal ganglion cells were retrogradely labeled after optic nerve deposits of biocytin to reveal their entire dendritic tree. Cebus M and P ganglion cell morphology revealed by biocytin retrograde filling is similar to that described for macaque and human M and P ganglion cells obtained by in vitro intracellular injection of HRP and neurobiotin. We measured 264 and 441 M and P ganglion cells, respectively. M ganglion cells have larger dendritic field and cell body size than P ganglion cells at any comparable temporal or nasal eccentricity. Dendritic trees of both M and P ganglion cells are smaller in the nasal than in the temporal region at eccentricities greater than 5 mm and 2 mm for M and P ganglion cells, respectively. The depth of terminal dendrites allows identification of both inner and outer subclasses of M and P ganglion cells. The difference in dendritic tree size between inner and outer cells is small or absent. Comparison between Cebus and Macaca shows that M and P ganglion cells have similar sizes in the central retinal region. The results support the view that M and P pathways are similarly organized in diurnal dichromat and trichromat primates.

Mosaics of neurons are usually quantified by methods based on nearest-neighbor distance (NND). The commonest indicator of regularity has been the ratio of the mean NND to the standard deviation, here termed the ‘conformity ratio.’ However, an accurate baseline value of this ratio for bounded random samples has never been determined; nor was its sampling distribution known, making it impossible to test its significance. Instead, significance was assessed from goodness-of-fit to a Rayleigh distribution, or from another ratio, that of the observed mean NND to an expected mean predicted by theory, termed the dispersion index. Neither approach allows for boundary effects that are common in experimental mosaics. Equally common are ‘missing’ neurons, whose effects on the statistics have not been studied. To address these deficiencies, random patterns and real neuronal mosaics were analyzed statistically. Ns independent random-point samples of size Np were generated for 13 Np values between 25 and 6400, where Ns × Np ≥ 144,000. Samples were generated with rectangular boundaries of aspect ratio 1:1, 1:5, and 1:10 to examine the influence of sample geometry. NND distributions, conformity ratios, and dispersion indices were computed for the resulting 45,997 independent random patterns. From these, empirical sampling distributions and critical values were determined. NND distributions for small-to-medium, bounded, random populations were shown to differ significantly from Rayleigh distributions. Thus, goodness-of-fit tests are invalid for most experimental mosaics. Charts are presented from which the significance of conformity ratios or dispersion indices can be read directly. The conformity ratio reacts conservatively to extremes of sample geometry, and provides a useful and safe test. The dispersion index is nonconservative, making its use problematic. Tests based on the theoretical distribution of the dispersion index are unreliable for all but the largest samples. Random deletions were also made from 33 real retinal ganglion cell mosaics. The mean NND, conformity ratio, and dispersion index were determined for each original mosaic and 36 independent samples at each of nine sampling levels, retaining between 90% and 10% of the original population. An exclusion radius, based on a spatial autocorrelogram, was also calculated for each of these 10,725 mosaic samples. The mean NND was moderately insensitive to undersampling, rising smoothly. The exclusion radius was remarkably insensitive. The conformity ratio and dispersion index fell steeply, sometimes failing to reach significance while half of the cells still remained. For the same 33 original mosaics, linear regression showed the exclusion radius to be 62 ± 3% of the mean NND.

Autoradiography with 125I-neurotensin in normal and enucleated hamsters was used to define the distribution of receptors for this peptide in the superficial layers of the superior colliculus (SC). Neurotensin binding sites were densely distributed in the stratum griseum superficiale (SGS), and results from the enucleated animals indicated that they were not located on retinal axons. The effects of neurotensin on individual superficial layer cells were tested in single-unit recording experiments. Neurotensin was delivered via micropressure ejection during visual stimulation (n = 75 cells), or during electrical stimulation of either the optic chiasm (OX; n = 47 cells) or visual cortex (CTX; n = 29 cells). In comparison with control values, application of neurotensin decreased visual responses of all SC cells tested to 54.1 ± 34.9% (mean ± standard deviation; range of decrement 7.5 to 100%; nine cells showed no effect or an increase in visual activity, which for four of these was ≥30%). Neurotensin application also reduced responses to electrical stimulation of either OX or CTX, respectively, to 65.8 ± 36.5% of control values (range of decrement 2.6 to 97.4%; 12 neurons showed a weak increment ≤ 30%) and 68.0 ± 38.5% (range of decrement 3.3 to 100%; five cells showed no effect or an increment, in one case ≥ 30%). Of the 25 neurons tested with both OX and CTX stimulation, the correlation of evoked response suppression by neurotensin was highly significant (r = 0.70; P < 0.001). This suggests that the suppressive effects of neurotensin were common to both pathways. To test whether the inhibitory effects of neurotensin were presynaptic or postsynaptic, Mg2+ ions were ejected iontophoretically to abolish synaptic responses, and the neurons (n = 16) were activated by iontophoresis of glutamate and then tested with neurotensin. Neurotensin reduced the glutamate-evoked responses to an average 59.3 ± 37.9% of control values (range 2.3 to 92.5%; one cell showed an increment >30%). This result suggests that the site of action of neurotensin is most likely postsynaptic.

We have examined the retinotopy in the superior colliculus of pigmented and albino ferrets using both anatomical and electrophysiological methods. While the distribution of contralaterally projecting retinotectal ganglion cells is characterized by the presence of an area centralis superimposed on a visual streak in both strains, the ipsilateral projection from temporal hemiretina is strongly reduced in albinos. In spite of the significantly altered retinotectal projection pattern, the collicular visual field map in the albino ferret reveals the same characteristics as in the pigmented animal with a strongly enlarged representation of the center of visual space. An areal comparison between retinotectal ganglion cell distribution and collicular areal magnification shows that the increase in areal magnification factor between the periphery and the representation of the central visual hemifield exceeds the corresponding increase in retinal ganglion cell density between peripheral retina and area centralis by a factor of three in pigmented and a factor of four in albino ferrets. The areal magnification factor of the representation of the retinal visual streak does not exceed the increase in retinotectal ganglion cell density. Thus, our results suggest that the representation of visual space in the superior colliculus of albino and pigmented ferrets does not simply follow the retinotectal ganglion cell density, but that there is an enhanced representation of the frontal central visual field. The possibility is discussed that the collicular visual field map may be determined either by both retinotectal and corticotectal projections or by the colliculus' intrinsic structure.