Strabismus (or squint) is both a well-established model for developmental plasticity of the brain and a frequent clinical symptom. While the layout and topographic relationship of functional domains in area 17 of divergently squinting cats has been analyzed extensively in recent years (e.g. Löwel et al., 1998), functional maps in convergently squinting animals have so far not been visualized with comparable detail. We have therefore investigated the functional organization of area 17 in adult cats with a surgically induced convergent squint angle. In these animals, visual acuity was determined by both behavioral tests and recordings of visual evoked potentials, and animals with comparable acuities in both eyes were selected for further experiments. The functional layout of area 17 was visualized using optical imaging of intrinsic signals. Monocular iso-orientation domains had a patchy appearance and their layout was different for left and right eye stimulation, so that segregated ocular dominance domains could be visualized. Iso-orientation domains exhibited a pinwheel-like organization, as previously described for normal and divergently squinting cats. Mean pinwheel density was the same in the experimental and control animals (3.4 pinwheel centers per mm2 cortical surface), but significantly (P < 0.00001) higher than that reported previously for normal and divergently squinting cats (2.7/mm2). A comparison of orientation with ocular dominance maps revealed that iso-orientation domains were continuous across the borders of ocular dominance domains and tended to intersect these borders at steep angles. However, in contrast to previous reports in normally raised cats, orientation pinwheel centers showed no consistent topographical relationship to the peaks of ocular dominance domains. Taken together, these observations indicate an overall similarity between the functional layout of orientation and ocular dominance maps in area 17 of convergently and divergently squinting cats. The higher pinwheel densities compared with previous reports suggest that animals from different gene pools might generally differ in this parameter and therefore also in the space constants of their cortical orientation maps.

It is well established that the responses of neurons in the lateral geniculate nucleus (LGN) can be modulated by feedback from visual cortex, but it is still unclear how cortico-geniculate afferents regulate the flow of visual information to the cortex in the primate. Here we report the effects, on the gain of LGN neurons, of differentially stimulating the extraclassical receptive field, with feedback from the striate cortex intact or inactivated in the marmoset monkey, Callithrix jacchus. A horizontally oriented grating of optimal size, spatial frequency, and temporal frequency was presented to the classical receptive field. The grating varied in contrast (range: 0–1) from trial to trial, and was presented alone, or surrounded by a grating of the same or orthogonal orientation, contained within either a larger annular field, or flanks oriented either horizontally or vertically. V1 was ablated to inactivate cortico-geniculate feedback. The maximum firing rate of LGN neurons was greater with V1 intact, but was reduced by visually stimulating beyond the classical receptive field. Large horizontal or vertical annular gratings were most effective in reducing the maximum firing rate of LGN neurons. Magnocellular neurons were most susceptible to this inhibition from beyond the classical receptive field. Extraclassical inhibition was less effective with V1 ablated. We conclude that inhibition from beyond the classical receptive field reduces the excitatory influence of V1 in the LGN. The net balance between cortico-geniculate excitation and inhibition from beyond the classical receptive field is one mechanism by which signals relayed from the retina to V1 are controlled.

Previous studies of human contrast adaptation employing visually evoked potentials (VEP) have revealed contradictory results, namely, either a reduction or an enhancement in VEP amplitude. In a cross-adaptation experiment, we explored the possibility that differences in the temporal frequency of adapting and test patterns played a role. Phase-reversing checkerboard stimuli [1-deg check size, temporal frequency 8.5 or 17 reversals per second (rps)] served as adaptation and test pattern with contrasts of 0 or 97%. In 13 subjects, we recorded both retinal (PERG) and cortical (VEP) steady-state responses simultaneously. In a balanced block design, all four combinations of the temporal adaptation and test frequencies were employed. Contrast adaptation reduced the PERG amplitude by about 20% in every temporal condition (P < 0.001). The VEP amplitude was strongly affected by adaptation, but the effect differed in magnitude and sign depending on condition: With identical adaptation and test frequency, amplitude was reduced by 15% (P = 0.07) at 8.5 rps and by 38% at 17 rps (P < 0.05). Adapting at 8.5 rps and testing at 17 rps had a tiny (14%) insignificant effect, whereas adapting at 17 rps and testing at 8.5 rps revealed an amplitude enhancement of 27% (P < 0.05). These strong temporal cross-adaptation effects (in the VEP, but not in the PERG) suggest that the adaptable cortical mechanisms (gain control) can be narrowly tuned in their temporal properties. A sizable adaptation effect can even change its sign when varying the temporal frequency by a factor of two. This finding resolves contradictions between previous VEP adaptation studies and reconciles them with psychophysical findings.

This study presents a morphological and quantitative analysis of displaced ganglion cells performed in the chick retina at different stages of development (E11, E17, & P2). The lipophilic dye DiI inserted into the optic nerve provided a complete staining of displaced ganglion cell population and of their dendritic trees. From 11 days of incubation (E11) all neurons present a uniform morphology and are unmistakably recognizable by the dimensions of their cell body and by the presence of the axon. Their dendritic arborizations shape a complex network through the retina. Cell bodies are randomly distributed but dendritic trees of neighboring cells constantly present two levels of dendritic overlap: about 50% of the cells present a high degree of overlap, more than the 30% up to 95% of their total area, while the other half overlaps less than 20%. The high degree of overlap identifies a cluster, which is regularly formed by three and more rarely by four neurons starting from 17 days of incubation (E17) onward and after birth. From E17 onward, 94% of clusters is constantly formed by three cells and 6% of the clusters by four neurons. The distribution and the spatial arrangement of clusters are very regular, forming a mosaic that gives rise to a precise retinal coverage. The nearest-neighbor analysis unequivocally demonstrated that the mosaic of clusters is the most regular array so far described. This exact arrangement starts from 11 days of incubation and is maintained and refined through the following stages of development and after birth.

Both dopamine and melatonin are important for the regulation of retinal rhythmicity, and substantial evidence suggests that these two substances are mutually inhibitory factors that act as chemical analogs of day and night. A circadian oscillator in the mammalian retina regulates melatonin synthesis. Here we show a circadian rhythm of retinal dopamine content in the mouse retina, and examine the role of melatonin in its control. Using high-performance liquid chromatography (HPLC), we measured levels of dopamine and its two major metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in retinas of C3H+/+ mice (which make melatonin) and C57BL/6J mice that are genetically incapable of melatonin synthesis. In a light/dark cycle both strains of mice exhibited daily rhythms of retinal dopamine, DOPAC, and HVA content. However, after 10 days in constant darkness (DD), a circadian rhythm in dopamine levels was present in C3H, but not in C57 mice. C57 mice given ten daily injections of melatonin in DD exhibited a robust circadian rhythm of retinal dopamine content whereas no such rhythm was present in saline-injected controls. Our results demonstrate that (1) a circadian clock generates rhythms of dopamine content in the C3H mouse retina, (2) mice lacking melatonin also lack circadian rhythms of dopamine content, and (3) dopamine rhythms can be generated in these mice by cyclic administration of exogenous melatonin. Our results also indicate that circadian rhythms of retinal dopamine depend upon the rhythmic presence of melatonin, but that cyclic light can drive dopamine rhythms in the absence of melatonin.

Disparity-tuned cells in primary visual cortex (V1) are thought to play a significant role in the processing of stereoscopic depth. The disparity-specific responses of these neurons have been previously described by an energy model based on local, feedforward interactions. This model fails to predict the response to binocularly anticorrelated stimuli, in which images presented to left and right eyes have opposite contrasts. The original energy model predicts that anticorrelation should invert the disparity tuning curve (phase difference π), with no change in the amplitude of the response. Experimentally, the amplitude tends to be reduced with anticorrelated stimuli and a spread of phase differences is observed, although phase differences near π are the most common. These experimental observations could potentially reflect a modulation of the V1 signals by feedback from higher visual areas (because anticorrelated stimuli create a weaker or nonexistent stereoscopic depth sensation). This hypothesis could explain the effects on amplitude, but the spread of phase differences is harder to understand. Here, we demonstrate that changes in both amplitude and phase can be explained by a straightforward modification of the energy model that involves only local processing. Input from each eye is passed through a monocular simple cell, incorporating a threshold, before being combined at a binocular simple cell that feeds into the energy computation. Since this local feedforward model can explain the responses of complex cells to both correlated and anticorrelated stimuli, there is no need to invoke any influence of global stereoscopic matching.

Alpha-2 adrenoceptor agonists have previously been shown to enhance neuronal survival in an optic nerve mechanical injury model and to protect photoreceptors in a light-induced degeneration model. The purpose of this study was to examine the effect of the alpha-2 adrenoceptor agonist in a pressure-induced retinal ischemia model. Brown-Norway rats were treated systemically or topically with alpha-2 adrenoceptor specific agonist brimonidine. Retinal ischemia was induced by increasing the intraocular pressure to 110 mm Hg for 50 min. The effect of brimonidine on retinal ischemic injury was functionally assessed in the rats 7 d later using electroretinography (ERG). Ischemia-induced retinal cell death was studied using the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining. We found that brimonidine treatment significantly protected the retina from retinal ischemic injury in a dose- and time-dependent manner. This protection can be achieved either by systemic or topical application and can be blocked by pretreatment with the alpha-2 adrenoceptor antagonist, yohimbine. Using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis, we found that brimonidine can up-regulate the expression of basic fibroblast growth factor, bcl-2 and bcl-xl in the retina. The drug also can activate two major cell survival signaling pathways in the retina: the extracellular-signal-regulated kinases (ERKs) and phosphatidylinositol-3′ kinase/protein kinase Akt pathways. All these aforementioned factors may potentially contribute in mediating brimonidine's protective effect in this acute retinal ischemia model.

We previously reported that two types of visual thalamic interneurons (class III and class V) could be distinguished by the presence or absence of the enzyme brain nitric oxide synthase (bNOS; Bickford et al., 1999). In the present study, we found that further immunocytochemical characterization can be used to isolate class V and class III neurons: class V neurons express GABA and bNOS but not the calcium binding protein calbindin, whereas class III neurons express GABA and calbindin, but not bNOS. By pairing staining for bNOS or calbindin with staining for GABA, we were able to distinguish class III and class V neurons, thereby allowing us to characterize the synaptic inputs to these two interneuron populations within the cat pulvinar nucleus. We found class III and class V interneurons participate in distinctly different circuitries. Class III cells receive the majority of their input from large terminals with round vesicles (RL profiles, that presumably originate from cortical layer V) while class V cells receive all of their input from small terminals with round vesicles (RS profiles, that presumably originate from cortical layer VI). These two types of interneurons also target different regions of the dendritic arbors of thalamocortical cells; class III cells contact large caliber (presumably proximal) thalamocortical dendrites within glomeruli, while class V cells contact the small caliber (presumably distal) thalamocortical cell dendrites within the extraglomerular neuropil. Thus, a dual inhibitory system exists within the visual thalamus that integrates different types of corticothalamic input and targets distinct regions of thalamocortical cell dendritic arbors.

We investigated the effects of group II metabotropic glutamate receptor (mGluR) activation on excitatory synaptic transmission in the salamander retinal slice preparation. The group II selective agonists DCG-IV and LY354740 reduced light-evoked excitatory postsynaptic currents (EPSCs) in ganglion cells. To determine the synaptic basis of this effect, we also recorded from bipolar cells and horizontal cells. In ON bipolar cells, DCG-IV increased the inward current in darkness but did not affect the peak current at light onset. In OFF bipolar cells and horizontal cells, DCG-IV had the opposite effect, reducing the inward current in darkness. Given the opposite polarities of these two classes of synapses, our results suggest that group II mGluRs act presynaptically to reduce glutamate release from photoreceptors. To determine whether DCG-IV affected rods or cones, we applied light stimuli that selectively activate each type of photoreceptor. In horizontal cells, most of which receive mixed synaptic input from rods and cones, DCG-IV reduced rod-driven EPSCs evoked by 470-nm stimuli and cone-driven EPSCs elicited by 700-nm stimuli in the presence of a rod-saturating background. Thus, activation of group II mGluRs reduced rod- and cone-mediated glutamate release. Our results suggest that group II mGluRs could mediate feedback by which extracellular glutamate inhibits glutamate release from photoreceptor terminals.

The responses of many ganglion cells in the rabbit retina are mediated, at least in part, by acetylcholine (ACh) acting on neuronal nicotinic acetylcholine receptors (nAChRs). nAChRs are comprised of α and β subunits; three β subunits and nine α subunits of nAChRs have been identified and these subunits can combine to form a large number of functionally distinct nAChR subtypes. We examined the effects of cholinergic agents on the light-evoked responses of ganglion cells to determine which nAChR subtypes mediate the effects of ACh. Extracellular recordings of retinal ganglion cells were made in intact everted eyecup preparations and nicotinic agonists and antagonists were added to the superfusate. While several ganglion cell classes exhibited methyllycaconitine (MLA) sensitivity, the directionally selective (DS) ganglion cells were most sensitive; exposure to 30 nanomolar MLA, a concentration reportedly too low to affect αBgt-insensitive nAChRs, suppressed the stimulus-evoked responses of DS cells without eliminating directional selectivity. Epibatidine, which at low concentrations is an agonist selective for αBgt-insensitive nAChRs, stimulated firing of various cell types including DS ganglion cells at low nanomolar concentrations. The effects of the various agents tested persisted under cobalt-induced synaptic blockade. The low nanomolar MLA and epibatidine sensitivity of DS cells suggests that DS ganglion cells express both αBgt-sensitive and αBgt-insensitive nAChRs. Other ganglion cell types appear to express only αBgt-sensitive nAChRs but not αBgt-insensitive nAChRs.

Limulus lateral eyes shed and renew a portion of their photosensitive membrane (rhabdom) daily. Shedding, in many species including Limulus, is regulated by complex interactions between circadian rhythms and light. Little is known about how circadian clocks and photoreceptors communicate to regulate shedding. Limulus photoreceptors do not contain an endogenous circadian oscillator, but rely upon efferent outflow from a central clock for circadian timing. To investigate whether the putative efferent neurotransmitter octopamine (OA) communicates circadian rhythms that prime the lateral eye for transient rhabdom shedding, we decoupled photoreceptors from the clock by transecting the lateral optic nerve (contains the retinal efferent fibers). Overnight (6 h) intraretinal injections of 40 μM OA restored transient shedding to lateral eyes with transected nerves to levels comparable to those of intact internal control eyes. To determine whether OA acts alone in communicating circadian rhythms that prime the lateral eye for transient shedding, we “primed” eyes with intact nerves for transient shedding with exogenous OA during subjective day. In nature, lateral eyes shed their rhabdoms only once a day at dawn following overnight efferent priming. Eyes in animals placed in darkness during subjective day, when the retinal efferents are quiescent, and injected for 6 h with 40 μM OA shed their rhabdoms in response to a second introduction to light. Untreated control eyes of the same animals did not. The same results were observed in vitro in lateral eyes treated similarly. Octopamine is the only efferent neurotransmitter/messenger required to make lateral eyes competent for transient shedding. Phentolamine, an OA receptor antagonist, reduced the number of photoreceptors primed for transient shedding and the amount of rhabdom shed in those photoreceptors suggesting that OA acts via a specific OA receptor.

The aim of this study was to determine whether agmatine, a channel permeable probe, can identify photoreceptor dysfunction in the Royal College of Surgeons (RCS) retina at an earlier stage to that shown by apoptosis or anatomical markers, and also characterize the neurochemical development of the inner retina in the normal and degenerating rat. We used isolated retinas at different ages incubated in physiological media containing agmatine. Subsequently, postembedding immunocytochemistry was used to determine the number of labelled photoreceptors and the labelling pattern within postreceptoral neurons. Agmatine labelling patterns revealed a sequential development of retinal neurons beginning at postnatal day (PND)11/12 with most horizontal cells, a few ganglion and amacrine cells, showing a strong signal. The neurochemical development progressed rapidly, and reflects to a large part the known distribution of glutamate receptors, with inner nuclear labelling being evident by PND14, continuing with the same pattern of labelling in adulthood for the control retina. The RCS retina showed markedly reduced agmatine labelling in the inner retina at PND20. A rapid increase in photoreceptor AGB labelling was evident during the degeneration phase. Multiple samples at PND14 and PND16 confirmed a significant increase of labelled photoreceptors in the RCS retina.

We used qualitative tests to assess the sensitivity of 1043 V2 neurons (predominantly multiunits) in anesthetised macaque monkeys to direction, length, orientation, and color of moving bar stimuli. Spectral sensitivity was additionally tested by noting ON or OFF responses to flashed stimuli of varied size and color. The location of 649 units was identified with respect to cycles of cytochrome oxidase stripes (thick-inter-thin-inter) and cortical layer. We used an initial 8-way stripe classification (4 stripes, and 4 “marginal” zones at interstripes boundaries), and a 9-way layer classification (5 standard layers (2–6), and 4 “marginal” strata at layer boundaries). These classes were collapsed differently for particular analyses of functional distribution; the main stripe-by-layer analysis was performed on 18 compartments (3 stripes × 6 layers). We found direction sensitivity only within thick stripes, orientation sensitivity mainly in thick stripes and interstripes, and spectral sensitivity mainly in thin stripes. Positive length summation was relatively more frequent in thick stripes and interstripes, and negative length/size summation in thin stripes. All these “majority” characteristics of stripes were most prominent in layers 3A and 3B. By contrast, “minority” characteristics (e.g. spectral sensitivity in thick stripes; positive size summation in thin stripes) tended to be most frequent in the outer layers, that is, layers 2 and 6. In consequence, going by the four functions tested, the distinctions between stripes were maximal in layer 3, moderate in layer 2, and minimal in layer 6.

Eye growth and refraction are regulated by visual processing in the retina. Until now, the messengers released by the retina to induce these changes are largely unknown. Previously, it was found that glucagon amacrine cells respond to defocus in the retinal image and even to its sign. The expression of the immediate-early gene product ZENK increased in this cell population in eyes wearing plus lenses and decreased in minus lens-treated chicks. Moreover, it was shown that the amount of retinal glucagon mRNA increased during treatment with positive lenses. Therefore, it seems likely that these cells contribute to the visual regulation of ocular growth and that glucagon may act as a stop signal for eye growth. The purpose of the present study was to accumulate further evidence for a role of glucagon in the visual control of eye growth. Chicks were treated with plus and minus lenses after injection of different amounts of the glucagon antagonist des-His1-Glu9-glucagon-amide or the agonist Lys17,18,Glu21-glucagon, respectively. Refractive development and eye growth were recorded by automated infrared photorefraction and A-scan ultrasound, respectively. The glucagon antagonist inhibited hyperopia development, albeit only in a narrow concentration range, and at most by 50%, but not myopia development. In contrast, the agonist inhibited myopia development in a dose-dependent fashion. At high concentrations, it also prevented hyperopia development.

We recorded activity of single units in macaque monkey primary visual cortex (V1) to define the retinotopic extent of the visual inputs that drive or modulate V1 neuron responses in parafoveal and peripheral (calcarine) cortex. We used high-contrast drifting grating stimuli to define the extent of the area over which responses summate and the extent of the receptive-field surround. We found responses of most V1 cells to summate over 1 deg, with a suppressive surround typically twice that in diameter, though for some cells (even in parafoveal V1) surrounds exceeded 13 deg in diameter. Surprisingly, we found no significant laminar differences in these dimensions or in the strength of surround suppression. We found that surround suppression in most cells arises from both the ends and sides of the receptive field. Our measures indicate that the strongest modulatory input arises from regions immediately adjacent to the excitatory summation area. These physiological measures suggest that the high-contrast summation field of V1 neurons can be accounted for by the sum of lateral geniculate nucleus (LGN) inputs offered to the local cortical column, with monosynaptic lateral connections within area V1 adding the larger dimensions of the low-contrast summation field and the near surround. Neither of these inputs suffice to explain the largest surrounds, which most likely derive from feedback from extrastriate visual areas.

The cellular responses of the cone-dominant ground squirrel retina to retinal detachment were examined and compared to those in rod-dominant species. Retinal detachments were made in California ground squirrels. The retinas were prepared for light, electron, and confocal microscopy. Tissue sections were labeled with antibodies to cone opsins, rod opsin, glial fibrillary acidic protein (GFAP), vimentin, synaptophysin, cytochrome oxidase, and calbindin D 28K. Wax sections were probed with the MIB-1 antibody to detect proliferating cells. By 10 h postdetachment many photoreceptor cells in the ground squirrel already show structural signs of apoptosis. At 1 day many photoreceptors have collapsed inner segments (IS), yet others still have short stacks of outer segment discs. At 3 days there is a marked increase in the number of dying photoreceptors. Rod and medium-/long-wavelength opsins are redistributed in the cell membrane to their synaptic terminals. At 7 days photoreceptor cell death has slowed. Some regions of the outer nuclear layer (ONL) have few photoreceptor somata. IS remnants are rare on surviving photoreceptors. At 28 days these trends are even more dramatic. Retinal pigmented epithelium (RPE) cells do not expand into the subretinal space. The outer limiting membrane (OLM) appears flat and uninterrupted. Müller cells remain remarkably unreactive; they show essentially no proliferation, only negligible hypertrophy, and there is no increase in their expression of GFAP or vimentin. Horizontal cells show no dendritic sprouting in response to detachment. The speed and extent of photoreceptor degeneration in response to detachment is greater in ground squirrel than in cat retina—only a small number of rods and cones survive at 28 days of detachment. Moreover, the almost total lack of Müller cell and RPE reactivity in the ground squirrel retina is a significant difference from results in other species.

The response properties of postreceptoral sensory neurones are determined by the properties of their input neurones, by intrinsic membrane properties, and by the properties of neurotransmitter receptors on the soma and dendritic tree. We previously showed that inhibitory neurotransmitter (GABAA and glycine) receptors on a well-characterised sensory neurone, the parasol ganglion cell in the primate retina, are segregated towards the distal part of the dendritic tree. Here we studied the distribution of excitatory ionotropic glutamate receptor subunits on the dendrites of parasol cells in the retina of a New World monkey, the marmoset, Callithrix jacchus. Individual ganglion cells were intracellularly injected in an in vitro retinal wholemount preparation. Ionotropic glutamate receptor subunits, including AMPA (GluR1-4), kainate (GluR6/7), NMDA (NR1C2′) subunits, and the orphan receptors δ1 and δ2 were visualized with immunocytochemical methods. Immunoreactive puncta that colocalized with the dendrites of ganglion cells were analyzed using standard and/or confocal light microscopy. Colocalized puncta were present on parasol dendrites for all subunits studied, but their density was much lower (approximately 1/5) than previously reported for inhibitory (GABA and glycine) receptors. Segregation of the glutamate receptor clusters (GluR1, GluR6/7 subunits) to the peripheral dendrites was less marked than that shown for GABA and glycine receptor clusters. No sign of segregation of colocalized puncta to the peripheral part of the dendritic field was seen with antibodies to the GluR2, GluR2/3, GluR4, δ1/2, or NR1C2′ subunits. The results suggest that although there is diverse expression of glutamate receptor subtypes, the glutamatergic synapses form only a small proportion of the total synaptic input to primate ganglion cells. They further suggest that the processes which control distribution of excitatory and inhibitory synapses on the dendritic field of ganglion cells are, at least to some extent, independent.

We examined the distribution and morphological types of ganglion cells in the retina of the zebrafish, a model vertebrate genetic organism. Using cresyl violet and methylene blue staining, a prominent central area was observed in the ventral temporal retina. The density of ganglion cell layer neurons averaged from ∼12,000/mm2 in the dorsal-nasal retina to a peak of ∼37,000/mm2 in the ventral-temporal retina. Individual zebrafish ganglion cells were labeled by backfilling with DiI through the optic nerve followed by reconstruction using confocal microscopy. The dendritic stratification and branching pattern of each labeled ganglion cell was examined in relation to the borders of the inner plexiform layer (IPL). We identified 11 different morphological types of ganglion cell. The most commonly labeled ganglion cells were two types termed Type III or IV, which displayed highly stratified dendritic arborizations in their respective ON-, OFF-sublaminae of the IPL. Their dendritic branching patterns were highly asymmetric with many thorn-like varicosities that profusely filled the area of arborization. In contrast, Type V cells formed a small simply branching dendritic field in the innermost portion of the ON-sublamina of the IPL. Two large ganglion cell types (Types I and II) with wide monostratified dendritic fields were found in both the ON- and OFF-sublamina of the IPL. Three different types of multistratified/bistratified ganglion cells were found (Types, IX, X, and XI.) whose dendrites occupied different regions of the IPL. The multistratified dendrites of IX cells occupied the whole width of the IPL, while the dendrites of Type XI cells formed vertical claw-like endings in only the ON-sublamina of the IPL. We conclude that zebrafish ganglion cells display a rich variety of types and branching patterns. This study establishes a series of baseline measurements of zebrafish ganglion cells to facilitate examination of genes playing a role in the specification and stratification of ganglion cell types.

We have examined the visuotopic organization of area V2 of macaque monkeys in relation to its modular construction, comprising repetitive cycles of stripes running perpendicular to the border with area V1. Receptive fields were plotted in anesthetised animals, mainly using long penetrations parallel to the V1 border crossing several stripes in dorsal V2 within the representation of paracentral, inferior visual field. We confirm that each set of modules (thick, thin, and interstripes) mounts an unbroken coverage of the visual field, since there is almost invariably some overlap between the aggregate fields recorded in successive stripes of the same class, at intervals of one cycle. Also as expected, penetrations perpendicular to the stripes record changes in eccentricity along an isopolar visual meridian. We measured the size of the point image along such an isopolar meridian in nine cases, and showed that on average it exceeds the length of a typical cycle; again, this implies that no point in space escapes analysis by any of the functional modules. The representation of eccentricity across a cycle of stripes resembles a “ratchet” model, in which the gradient of eccentricity across a single stripe exceeds the gradient across the full cycle, leading to discontinuities (“switchbacks”) at the borders between stripes. The shift in eccentricity across the width of a stripe is sufficient to maintain a virtually continuous map across successive stripes of the same class; when coupled to receptive field scatter about the mean trend, this creates the overlap of aggregate fields.

The resistances of the horizontal cell syncytium in the vertebrate retina are modulated in a time-dependent fashion during light stimulation. Therefore, the spatial properties of horizontal cells are expected to change with time after the illumination conditions are altered. This study was designed to investigate time- and intensity-dependent changes in the receptive-field properties of L1-type horizontal cells in the turtle Mauremys caspica. Photoresponses were elicited by monochromatic (650 nm) light stimuli of 2-s duration covering retinal spots of different radii. The length constants were derived from the relationships between amplitude and spot radius that were constructed for different time intervals after onset of the light stimulus. For a given stimulus intensity, the length constant transiently increased to a peak value and then slowly recovered to a plateau level. When the length constant was compared to the amplitude of the response to full-field illumination for the entire duration of the light stimulus, an ellipse-like curve was obtained indicating that for a given membrane potential, two different values of the length constant could be obtained. Dopamine considerably reduced the size of the receptive fields but did not affect the time-dependent changes in the length constant. These results indicate that changes in the membrane resistance underlie short-term modulation of the receptive-field properties of turtle L1-type horizontal cells after onset of a light stimulus.