Cells of the cat's perigeniculate nucleus (PGN), part of the visual sector of the thalamic reticular nucleus (TRN), provide GABAergic inhibition to the A and A1 layers of the dorsal lateral geniculate nucleus (LGNd) and, therefore, may control information flow from the retina to the cortex. Previous electrophysiological experiments suggested that the PGN may be subdivided on the basis of ocular dominance thus reflecting the afferent and efferent projections with lamina A and A1 of the LGNd. The present study utilized the ability of wheat germ agglutinin-horseradish peroxidase (WGA-HRP) to be transported transneuronally following intraocular injections in four cats to examine whether there is any anatomical evidence for eye specific layers within the PGN. Sections were processed with tetramethylbenzidine. Light WGA-HRP transneuronal labeling of LGNd collaterals and somata were seen in the PGN and very light labeling (but not somata) was seen in the TRN. Neither the cells of the PGN projecting to the LGNd nor the LGNd relay collaterals within the PGN were clearly organized into nonoverlapping laminae related to the eye specific layers of the LGNd. However, parts of the PGN immediately adjacent to the LGNd appear devoid of connections with lamina A1 thus creating a thin monocular segment for the contralateral eye.

The retina of the leopard frog projects topographically to the superficial neuropil of the entire contralateral tectum. In the rostromedial neuropil of the tectum, there is a map of the binocular region of the visual field seen from the ipsilateral eye that is in register with the map of the binocular region of the visual field seen from the contralateral eye. The ipsilateral eye projects indirectly to the tectum through nucleus isthmi (n. isthmi), a midbrain tegmental structure. N. isthmi receives input from the ipsilateral optic tectum and sends projections bilaterally that cover both tectal lobes. Previous workers have not been able to find visual activity from the ipsilateral eye in the caudolateral optic tectum, representing the monocular visual field of the contralateral eye. We show electrophysiologically that across the entire extent of n. isthmi there are two superimposed maps, one map representing the entire visual field of the contralateral eye, the other map representing the binocular visual field of the ipsilateral eye. We also studied the behavioral consequences of localized lesions to n. isthmi and compared them to the behavioral consequences of localized lesions to the optic tectum representing equivalent areas of the visual field. Lesions to the optic tectum produce scotomas in the corresponding portion of the visual field. Lesions to n. isthmi, even medial n. isthmi representing the superior visual field, lead to scotomas in the temporal-most portion of the contralateral ground level visual field. Thus, the representation of visual space in n. isthmi is not a simple copy of the tectal representation of visual space.

The four spectral cone types in the zebrafish retina each contribute to photopic visual sensitivity as measured by the b-wave of the electroretinogram (ERG). The goal of the current study was to evaluate a model of photopic b-wave spectral sensitivity in the zebrafish that mapped first-order cellular and biophysical aspects of cone photoreceptors (visual pigment absorbance spectra and cone fractions) onto a second-order physiological aspect of cone-derived neural activity in the retina. Good correspondence between the model and photopic ERG data was attained using new visual pigment absorbance data for zebrafish cones (λmax of the L, M, and S cones were 564, 473, and 407 nm, respectively), visual pigment templates, and linearly gained cone fractions. The model inferred four distinct cone processing channels that contribute to the photopic b-wave, two of which are antagonistic combinations of cone-derived signals (L-M and M-S), and two of which are noncombinatorial signals from S and U cones. The nature of the gains and the processing channels suggested general rules of cone-specific inputs to second-order neurons. The model further suggested that the zebrafish retina utilizes neuronal mechanisms for enhancing sensitivity to luminance contrast at short wavelengths and chromatic contrast at middle and long wavelengths. The results indicated that first-order cellular and biophysical aspects of cone photoreceptors can successfully explain physiological aspects of cone-derived neuronal activity in the zebrafish retina.

Visual information is encoded at the photoreceptor synapse by modulation of the tonic release of glutamate from one or more electron-dense ribbons. This release is highest in the dark, when photoreceptors are depolarized, and decreases in grades when photoreceptors hyperpolarize with increasing light. Functional diversity between neurons postsynaptic at the synaptic ribbon arises in part from differential expression of both metabotropic (G-protein-gated) and ionotropic (ligand-gated) glutamate receptor. In the brain, different subunits also modulate the presynaptic active zone. In hippocampus, ionotropic kainate receptors localize to the presynaptic membrane of glutamatergic axon terminals and facilitate depolarization of the synapse (e.g. Lauri et al., 2001). Such facilitation may be helpful in the retina, where consistent depolarization of the photoreceptor axon terminal is necessary to maintain glutamate release in the dark. We investigated whether such a mechanism could be present in primate retina by using electron microscopy to examine the localization of the kainate subunits GluR6/7 at the rod axon terminal, where only a single ribbon synapse mediates glutamate release. We scored 54 rod axon terminals whose postsynaptic space contained one or more GluR6/7-labeled processes and traced these processes through serial sections to determine their identity. Of 68 labeled processes, 63% originated from narrow “fingers” of cytoplasm extending from the presynaptic axon terminal into the postsynaptic cleft. Each rod terminal typically inserts 4–6 presynaptic fingers, and we scored several instances where multiple fingers contained label. Such consistency suggests that each presynaptic finger expresses GluR6/7. The physiological properties of kainate receptors and the geometry of the rod axon terminal suggest that presynaptic GluR6/7 could provide a steady inward current to maintain consistent depolarization of the rod synapse in the long intervals between photons in the dark.

Certain ganglion cells in the mammalian retina are known to express a cGMP-gated cation channel. We found that a cGMP-gated current modulates spike responses of the ganglion cells in mammalian retinal slice preparation. In such cells under current clamp, bath application of the membrane-permeant cGMP analog (8-bromo-cGMP, 8-p-chlorophenylthio-cGMP) or a nitric oxide donor (sodium nitroprusside, S-nitroso-N-acetyl-penicillamine) depolarized the membrane potential by 5–15 mV, and reduced the amount of current needed to evoke action potentials. Similar effects were observed when the membrane potential was simply depolarized by steady current. The responses to cGMP are unaffected by inhibitors of cGMP-dependent protein kinase and Ca2+/calmodulin-dependent protein kinase. The response to cGMP persisted in Ca2+-free bath solution with Ca2+ buffers in the pipette. Under voltage clamp, cGMP analogs did not affect the response kinetics of voltage-gated currents. We conclude that cGMP modulates ganglion cell spiking simply by depolarizing the membrane potential via the inward current through the cGMP-gated channel. Modulation of this channel via the long-range NO-synthase amacrine cell may contribute to control of contrast gain by peripheral mechanisms.

APB (DL-2-amino-4-phosphonobutyric acid) has been found to affect the retinal processing of many vertebrate species as evidenced by the suppression of the b-wave component of the electroretinogram (ERG). The present study examined the effects of APB on the cone contributions to the ERG response of adult zebrafish (Danio rerio). ERG responses were obtained from light-adapted adult zebrafish following intravitreal injection of either saline alone or saline with various concentrations of APB ranging from 10 μm to 500 μM. Visual stimuli were 200-ms flashes of various wavelengths and irradiances. Spectral sensitivity functions were calculated from the irradiance versus response amplitude functions of the a-, b-, and d-wave components of the ERG response. Saline had no effects on the ERG response. However, APB had differential effects on the sensitivity of the b- and d-wave components. The effects of APB on the b-wave component were most apparent in the ultraviolet and short-wavelength portions (320–440 nm) of the spectral sensitivity function, although the b-wave was not completely eliminated at these wavelengths. APB-treated subjects were found to possess the same cone mechanisms (L-M and M-S) in the middle- and long-wavelength areas of the spectrum as saline injected subjects, although absolute sensitivity was lower for the APB-injected subjects. Spectral sensitivity based on the d-wave response was affected by APB but only in the short-wavelength region. All results appear to be independent of the APB dose. These results support the notion that glutamate receptors play a specific role in zebrafish visual processing. In addition, the effects of APB support recent anatomical evidence that the zebrafish retina may possess different types of glutamate receptors.

The ventral intraparietal area (VIP) is located at the end of the dorsal stream. Its neurons are known to have receptive-field characteristics similar to those of MT and MST neurons, but little is known about the temporal characteristics of VIP cells' responses. How fast are directionally selective responses evoked in the ventral intraparietal area after viewing optic flow patterns, and what are the temporal properties of these neuronal responses? To examine these questions, we recorded the activity of 37 directionally selective ventral intraparietal area (VIP) neurons in two awake macaque monkeys in response to optic flow stimuli with presentation times ranging from 17 ms to 2000 ms. We found a minimum response latency of 45 ms, and a median latency of 152 ms. Of all neurons, 10% showed early response components only (response latency < 150 ms and no activity in 500–2000 ms interval after stimulus onset), 55% only late response components (response latency >150 ms and sustained activity in 500–2000 ms interval), and 35% both early and late response components. Early responses appeared to very brief stimulus presentations (33-ms duration), while the late responses required longer stimulus durations. The directional selectivity was independent of optic flow duration in all cells. These results suggest that only a subset of neurons in area VIP may contribute to the fast processing of optic flow, while showing that the temporal properties of VIP responses clearly differ from the temporal characteristics of neurons in areas MT and MST.

High levels of endogenous cholecystokinin (CCK) are present in the rat retina (Eskay & Beinfeld, 1982), but the cellular localization and physiological actions of CCK in the rat retina are uncertain. The goals of this study were to characterize the cells containing CCK, identify cell types that interact with CCK cells, and investigate the effects of CCK on rod bipolar cells. Rat retinas were labeled with antibody to gastrin-CCK (gCCK) using standard immunofluorescence techniques. Patch-clamp methods were used to record from dissociated rod bipolar cells from rats and mice. Gastrin-CCK immunoreactive (-IR) axons were evenly distributed throughout the retina in stratum 5 of the inner plexiform layer of the rat retina. However, the gCCK-IR somata were only detected in the ganglion cell layer in the peripheral retina. The gCCK-IR cells contained glutamate decarboxylase, and some of them also contained immunoreactive substance P. Labeled axons contacted PKC-IR rod bipolar cells, and recoverin-IR ON-cone bipolar cells. CCK-octapeptide inhibits GABAC but not GABAA mediated currents in dissociated rod bipolar cells.

We report a unique anomaly in the ocular dominance column pattern of a single, normally pigmented macaque monkey. The column pattern contained large monocular areas inserted between the normal columns and the dorsal V1 border. These monocular regions received transneuronal input from the contralateral eye, indicating that a small population of temporal ganglion cells erroneously decussated at the optic chiasm. Projection of the column pattern back onto the visual field showed that the monocular wedges represented a ∼5-deg sector of ipsilateral field. This corresponded to the extent of naso-temporal overlap of ganglion cells in the normal retina, suggesting an error in axon guidance affecting cells close to the vertical midline of the retina. The consequences of the crossing error in this animal were threefold: it produced an anomalous monocular zone near the V1 border, the vertical meridian was not represented at the V1 border, and points near the vertical meridian were represented twice in the brain, once in each hemisphere.

(Article appeared in Visual Neuroscience (2002), 19, 257–264.)

Due to a production error, we are reprinting the following article because the color images were printed in black and white. The color images are so very important to the understanding of this article, we are reprinting it here with the color images in place.