To investigate the physiology and plasticity of mixed rod–cone ON-bipolar cells (Mb) in the goldfish retina, we established a slice preparation which allows us to optically monitor the synaptic activity of bipolar cell axon terminals. We used the styryl dye FM1-43 which is incorporated into active axon terminals due to synaptic vesicle cycling and thus reflects synaptic activity. Different activity states of the axon terminals were revealed when slices prepared from light-adapted retinae were incubated in the presence of FM1-43 under various conditions. Depolarizing high K+ Ringer (50 mM) and the gamma-butyric acid (GABA) antagonist bicuculline (100 μM) resulted in more than two-fold increase in the number of stained terminals compared to slices stained in normal Ringer. In contrast, GABA treatment (0.5 mM) reduced the frequency of stained terminals. Thus, in light-adapted retinal slices the synaptic activity of Mb axon terminals can be modulated towards higher and lower activity states. The fact that the GABA antagonist bicuculline had similar effects as stimulatory high K+ Ringer suggests that inhibitory control is an important component in the regulation of synaptic activity and transmitter release in Mb terminals.

Embryonic chick retinal pigment epithelial (RPE) cells can undergo transdifferentiation upon appropriate stimulation. For example, basic fibroblast growth factor (bFGF) induces intact RPE tissue younger than embryonic day 4.5 (E4.5) to transdifferentiate into a neural retina. NeuroD, a gene encoding a basic helix-loop–helix transcription factor, triggers de novo production of cells that resemble young photoreceptor cells morphologically and express general neuron markers (HNK-1/N-CAM and MAP2) and a photoreceptor-specific marker (visinin) from cell cultures of dissociated E6 RPE (Yan & Wang, 1998). The present study examined whether bFGF will lead to the same transdifferentiation phenomenon as neuroD when applied to dissociated, cultured E6 RPE cells, and whether interplay exists between the two factors under the culture conditions. Dissociated E6 RPE cells were cultured in the presence or absence of bFGF, and with or without the addition of retrovirus expressing neuroD. Gene expression was analyzed with immunocytochemistry and in situ hybridization. Unlike neuroD, bFGF did not induce the expression of visinin, or HNK-1/N-CAM and MAP2. However, bFGF elicited the expression of RA4 immunogenicity; yet, many of these RA4-positive cells lacked a neuronal morphology. Addition of bFGF to neuroD-expressing cultures did not alter the number of visinin-expressing cells; misexpression of neuroD in bFGF-treated cultures did not change the number of RA4-positive cells, suggesting the absence of interference or synergistic interaction between the two factors. Our data indicated that bFGF and neuroD induced the expression of different genes in cultured RPE cells.

Recurrent projections comprise a universal feature of cerebral organization. Here, we show that the corticofugal projections from the striate cortex (V1) to the lateral geniculate nucleus (LGN) robustly and multiplicatively enhance the responses of parvocellular neurons, stimulated by gratings restricted to the classical receptive field and modulated in luminance, by over two-fold in a contrast-independent manner at all but the lowest contrasts. In the equiluminant plane, wherein stimuli are modulated in chromaticity with luminance held constant, such enhancement is strongly contrast dependent. These projections also robustly enhance the responses of magnocellular neurons but contrast independently only at high contrasts. Thus, these results have broad functional significance at both network and neuronal levels by providing the experimental basis and quantitative constraints for a wide range of models on recurrent projections and the control of contrast gain.

Previous studies show that glycine transporter-1 (glyt-1) is a consistent membrane marker of adult retinal neurons that are likely to release glycine at their synaptic terminals (Pow, 1998; Vaney et al., 1998; Pow & Hendrickson, 1999). The current study investigated when glyt-1 immunoreactivity appeared in the postnatal rat retina, and whether all glycine-containing neurons also labelled for glyt-1. Ganglion cells, horizontal cells, and photoreceptors showed transient labelling. Many cells in the ganglion cell layer are immunoreactive for both glycine and glyt-1 at postnatal day (Pd) 1 but both are minimal by Pd5. Transient immunoreactivity for both glyt-1 and glycine was observed in presumptive horizontal cells between Pd5 and Pd10. At Pd1 many cells in the outer part of the retina which resembled immature photoreceptors were heavily labelled for glycine, but did not express glyt-1; these disappeared at older ages. These findings suggest diverse mechanisms and transient roles for glycine in the developing rat retina. In the adult rat retina, a subpopulation of amacrine cells are prominently immunoreactive for both glycine and glyt-1. These cells labelled for glycine at Pd1, but did not express significant levels of glyt-1 until Pd5. Processes from these amacrine cells did not reach the inner half of the inner plexiform layer until Pd10–14. Bipolar cells became glycine-IR between Pd10 and Pd14, but consistently lacked any glyt-1 immunoreactivity. This temporal pattern of labelling strongly indicates that bipolar cells label for glycine when gap junctions become functional between glycine/glyt-1 immunoreactive amacrine cells and cone bipolar cells.

Membrane voltage was recorded in rod photoreceptors in retina isolated from macaque monkey. The size of the single photon response and the magnitude of membrane voltage fluctuations were assessed in dark- and light-adapted retina. The “dark light” rate ID, defined as the rate of spontaneous photopigment isomerizations that would produce a variance equivalent to that of the noise measured in the dark, was calculated after matched filtering. The average value of 0.08 s−1 fell at the higher end of psychophysical estimates of dark light in human observers. In light-adapted rods the photon response decreased in amplitude and duration, and the magnitude of the voltage fluctuations increased with increasing background light intensity. The signal-to-noise ratio (SNR) for single rods was defined as the ratio of the peak amplitude of the photon response to the standard deviation of the noise fluctuations. The signal-to-noise ratio for dark-adapted rods SNRD was about 7. With increasing background intensity I, the SNR fell as SNRD(1 + I/ID)−1/2. This function may account for the increment thresholds measured with small brief test flashes in human psychophysical experiments.

Heme oxygenase-2 (HO-2) synthesizes carbon monoxide (CO), a modulator of soluble guanylate cyclase (sGC). To examine this signal transduction pathway in the retina, we immunocytochemically localized HO-2, and investigated the effects of CO on cGMP levels. In turtle, HO-2-like immunoreactivity (-LI) was in all photoreceptors, some amacrine cells, and in numerous bipolar and ganglion cells. HO-2-LI colocalized with sGC activity in many cells. In rat, HO-LI was found only in the inner retina, in ganglion and amacrine cells. In turtle, stimulation with CO alone primarily increased cGMP-LI in bipolar cells in the visual streak. Stimulation with a combination of CO and nitric oxide (NO) dramatically increased cGMP-LI throughout the retina, in comparison to the smaller increases seen with NO or CO alone. These data suggest that CO is an endogenous modulator of the sGC/cGMP signaling pathway in many retinal neurons, and can dramatically amplify NO-stimulated increases in cGMP.

In the absence of a direct and specific marker for basket cells, the aim of this paper was to use available data to estimate the density of basket cell synaptic input to smooth and spiny neurons within layer IV of cat striate visual cortex (area 17). A linear quantitative analysis of layer IV basket cell connectivity data suggests that on average basket cells (1) comprise 25–35% of all GABAergic neurons in layer IV (3552–4736 cells mm−3), (2) account for 30–41% of all putative inhibitory dendritic synapses of layer IV spiny stellate cells (145–195 synapses cell−1) and a similar proportion of layer IV basket cells (25–37%, 71–107 synapses cell−1), and (3) provide each layer IV spiny cell with 13–45 axons and each layer IV basket cell with 6–29 axons. These estimates suggest that basket cells may be less common and provide a smaller proportion of the dendritic synaptic input to layer IV spiny and smooth neurons than previously thought. In addition, the analysis indicates that a layer IV spiny stellate cell may receive on average as many synapses and axons from layer IV basket cells as from lateral geniculate relay cells. Based on this potential numerical similarity, a geniculate-basket synaptic pairing in a spine-shaft microcircuit is hypothesized. This microcircuit could implement a type of local (dendritic) push–pull interaction underlying subfield antagonism.

Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the retina and also appears to act as a trophic factor regulating photoreceptor development and regeneration. Although the tiger salamander is a major model system for the study of retinal circuitry and regeneration, our understanding of GABA receptors in this species is almost exclusively based on the results of physiological studies. Therefore, we have examined the pharmacological binding properties of GABAA receptors and their anatomical localization in the tiger salamander retina. Radioligand-binding studies showed that specific 3H-GABA binding to GABAA receptors was dominated by a single high-affinity binding site (Kd = 15.6 ± 6.9 nM). Specific binding of 3H-GABA was almost completely eliminated by muscimol (Ki = 105 ± 62 nM) and bicuculline (Ki = 14.3 ± 2.2 μM); however, SR-95531 only displaced about 40% of specific 3H-GABA binding (Ki = 35.0 ± 3.8 nM). These data indicate that there are at least two subtypes of GABAA receptors present in the salamander retina that can be distinguished by their antagonist binding properties: one sensitive to both bicuculline and SR-95531, and one sensitive to bicuculline but insensitive to SR-95531. Because localization of GABA receptors in the salamander retina by immunocytochemistry is problematic, GABAA receptors were localized by fluorescent ligand binding combined with immunocytochemical labeling for cell specific markers. Binding of fluorescently labeled muscimol to GABAA receptors was present in both plexiform layers and on photoreceptor cell bodies. GABAA receptors in the outer plexiform layer were localized to both photoreceptor terminals and horizontal cell processes.

Previous research in adults has demonstrated the utility of the visual evoked potential (VEP) to measure the integrity of the chromatic and achromatic visual pathways. The VEP has also been shown to be a valuable indicator of maturation of these pathways in infants up to 1 year of age. The present manuscript reports changes in the visual pathways from 2 years to adulthood as measured by the spatio-chromatic VEP. The responses to achromatic reversal stimuli designed to preferentially activate the low spatial-frequency achromatic (luminance) pathways appear adult-like by 1 year of age. The responses to low spatial-frequency isoluminant onset stimuli designed to preferentially activate the chromatic pathway do not appear as they do in the adult until after 12–13 years of age. The shapes of the chromatic VEP waveforms shift from a positive–negative complex to a negative–positive complex. These changes can be modeled by a decrease in the latency of a large negative component between the ages of 1 year and adulthood. The results suggest that for low spatial-frequency stimuli, there are long-term changes in the development of the chromatic pathways that are not observed in the low spatial-frequency achromatic pathways. The changes in the chromatic VEP waveforms with age may be a physiological correlate of reported behavioral changes.

Strabismus induces an abnormal pattern of alternating light and dark columns of cytochrome oxidase (CO) activity in macaque striate cortex. This pattern may arise because visual perception is suppressed in one eye to avoid diplopia. To test whether CO activity is reduced in the ocular dominance columns of the suppressed eye, we performed monocular enucleation to co-label the ocular dominance columns with Zif268 immunohistochemistry in seven exotropic adult Macaca fascicularis. This approach was unsuccessful, for two reasons. First, Zif268 yielded inconsistent labelling, that was usually greater in the enucleated eye's ocular dominance columns, but was sometimes greater in the intact eye's columns. Therefore, Zif268 was not a reliable method for identifying the ocular dominance columns serving each eye. Second, in three control animals we found that a brief survival period following monocular enucleation (needed for Zif268 levels to change) was long enough to alter CO staining. For example, a survival time of only 3 h was sufficient to induce CO columns, indicating that the activity of this enzyme fluctuates more rapidly than realized previously. Independent of these findings, we have also discovered that acute monocular enucleation produces a vivid pattern of ocular dominance columns visible in unstained or CO-stained sections under dark-field illumination. The ocular dominance columns of the acutely enucleated eye appear dark. This was verified by labelling the ocular dominance columns with [3H]proline. Dark-field illumination of the cortex after acute monocular enucleation offers a new, easy method for identifying the ocular dominance columns in macaques.

Atropine has previously been found to suppress visually induced myopia both in animals and humans. The mechanism of its action is unclear. We have studied its retinal effects in an in vitro preparation, using the retina-pigment epithelium-choroid complex of the chick eye. In vivo, deprivation myopia was induced by translucent goggles. Atropine solution was injected into the vitreous at two-day intervals. Dopamine release from the retina following atropine injection in vivo and from the in vitro retina preparation was quantified by HPLC-EC. In vitro preparations of the isolated chick retina–pigment epithelium–choroid were superfused with atropine. Light-induced potentials (local ERG), slow standing potentials from the retinal pigment epithelium/neural retina, and extracellular potassium concentrations were recorded. In line with previous findings, intravitreal injections of atropine (25 μg, 250 μg) reduced deprivation myopia in a dose-dependent manner. Atropine increased the release of the neurotransmitter dopamine into the superfusate in vitro at 100–500 μM and into the vitreous in vivo at 250 μg. Before an increase was measured in the vitreous, the retinal dopamine content was elevated. In concentrations equivalent to the intravitreal concentration to suppress myopia in vivo (200–800 μM), atropine induced spreading depression (SD) in the in vitro preparation. In contrast, muscarinic agonists, acetylcholine and pilocarpine, did not induce SD. Atropine reduced the ERG b- and d-wave, led to damped oscillations of RPE potentials, and reversed the ERG c-wave. Atropine suppressed myopia only at doses at which severe nonspecific side effects were observed in the retina. Atropine seems to intrude massively into the vital functions of the retina as indicated by the occurrence of SD. We conclude that atropine, by inducing SD, boosts neurotransmitter release from cellular stores, which may cancel out a presumed retinal signal that controls eye growth and through this, myopia.

Vertebrate vision starts with photoisomerization of the 11-cis-retinal chromophore to all-trans-retinal. Biosynthesis of 11-cis-retinal is required to maintain vision. A key enzyme catalyzing the oxidation of 11-cis-retinol is 11-cis-retinol dehydrogenase (11-cis-RDH), which is encoded by the RDH5 gene. 11-cis-RDH is expressed in the RPE and not in the neural retina. The consequences of a lack of 11-cis-RDH were studied in a family with fundus albipunctatus. We identified the causative novel RDH5 mutation, Arg157Trp, that replaces an amino acid residue conserved among short-chain alcohol dehydrogenases. Three-dimensional structure modeling and in vitro experiments suggested that this mutation destabilizes proper folding and inactivates the enzyme. Studies using RPE membranes indicated the existence of an alternative oxidizing system for the production of 11-cis-retinal. In vivo visual consequences of this null mutation showed complex kinetics of dark adaptation. Rod and cone resensitization was extremely delayed following full bleaches; unexpectedly, the rate of cone recovery was slower than rods. Cones showed a biphasic recovery with an initial rapid component and an elevated final threshold. Other unanticipated results included normal rod recovery following 0.5% bleach and abnormal recovery following bleaches in the 2–12% range. These intermediate bleaches showed rapid partial recovery of rods with transitory plateaux. Pathways in addition to 11-cis-RDH likely provide 11-cis-retinal for rods and cones and can maintain normal kinetics of visual recovery but only under certain constraints and less efficiently for cone than rod function.

We evaluated the generality of two models of vertebrate phototransduction. The approach was to quantitatively optimize each model to the full waveform of high-quality, dark-adapted (DA), salamander rod flash responses. With the optimal parameters, each model was then used to account for signature, qualitative features of rod responses from three experimental paradigms (stimulus/response, “S/R suite”): (1) step responses; (2) the intensity dependence of the period of photocurrent saturation (Tsatvs. ln(I)); and (3) light-adapted (LA) incremental flash sensitivity as a function of background intensity. The first model was the recent successful model of Nikonov et al. (1998). The second model replaced the instantaneous Ca2+ buffering used in the Nikonov et al. model with a dynamic buffer. The results showed that, in the absence of the dynamic Ca2+ buffer, the Nikonov et al. model does not have sufficient flexibility to provide a good fit to the flash responses, and, using the same parameters, reproduce the salient features of the S/R suite—critical features at step onset and offset are absent; the Tsat function has too shallow a slope; and the model cannot generate the empirically observed I-range of Weber–Fechner LA behavior. Some features could be recovered by changing parameters, but only at the expense of the fit to the reference (Ref) data. When the dynamic buffer is added, the model is able to achieve an acceptable fit to the Ref data while reproducing several features of the S/R suite, including an empirically observed Tsat function, and an extended range of LA flash sensitivity adhering to Weber's law. The overall improved behavior of the model with a dynamic Ca2+ buffer indicates that it is an important mechanism to include in a working model of phototransduction, and that, despite the slow kinetics of amphibian rods, Ca2+ buffering should not be simulated as an instantaneous process. However, neither model was able to capture all the features with the same parameters yielding the optimal fit to the Ref data. In addition, neither model could maintain a good fit to the Ref data when five key biochemical parameters were held at their current known values. Moreover, even after optimization, a number of important parameters remained outside their empirical estimates. We conclude that other mechanisms will need to be added, including additional Ca2+-feedback mechanisms. The present research illustrates the importance of a hybrid qualitative/quantitative approach to model development, and the limitations of modeling restricted sets of data.

There were three objectives to the work undertaken for this paper: (1) to provide a comprehensive characterization of the statistical properties of arrays of β-cell somata; (2) to develop a model that simulates cellular arrays with the same properties; and (3) to use this model to examine whether the array of β-cells should be viewed as one array or as two arrays, one each for its OFF- and ON-center cells. β-cells are morphological correlates of the electrophysiological X-cells and those β-cells whose dendrites stratify within the outer and inner sublamina of the retina's inner plexiform layer correspond, respectively, to OFF- and ON-center X-cells. Arrays of peripheral β-cell somata from two retinas were studied. A Delaunay triangulation and a Voronoi tessellation were generated for each array and measures derived from these constructs used to analyze the arrays' spatial organization. As others have shown previously with a less complete statistical characterization, we found that the arrays of OFF- and ON-center β-cells have similar spatial properties and are more regular than the array of all β-cells. We developed a model to simulate cellular arrays with spatial properties like those of arrays of β-cells. A good fit between model and real arrays was found when the model assumed an explicit spatial dependence between the placement of OFF- and ON-center cells. We propose therefore that a single array of β-cells formed of both OFF- and ON-center cells is consistent with the data currently available for β-cell somatic arrays.

The activity of the endogenous retinal dopamine (DA) pathway has been examined in the pigmented rat using retinas obtained from normal adult (∼3 months) and senile adults (∼24 months) using an in vitro electrophysiological approach. By comparing the pharmacological sensitivity of the horizontal cells (HCs) to exogenous DA, a D1 receptor antagonist (SCH 23390) and a DA-transport inhibitor (nomifensine), it is suggested that there is a functional deficit in the endogenous DA activity in the senile retina. Cells recorded from retinae obtained from senile animals are more sensitive to exogenous DA, whilst the senile retina is insensitive to SCH 23390. In addition, nomifensine was effective in potentiating subthreshold DA applications, but only in the normal adult retina. The data may suggest that endogenous DA release upon the HCs and selective re-uptake are suppressed in these retinae. These functional deficits also appear to be associated with changes in the receptive fields of the HCs, suggesting there is a corresponding deficit in spatial processing at the outer plexiform layer (OPL) of the senile rat.

Under photopic illumination conditions, motion detection in goldfish is dominated by the long-wavelength-sensitive cone type (L-cone), and under scotopic conditions motion it is determined by rods (Schaerer & Neumeyer, 1996). The switch from rod-dominated to cone-dominated motion detection occurs during light adaptation. It has been suggested that dopamine acts as a neuronal light-adaptative signal. It is known that dopamine affects wavelength discrimination through D1-dopamine receptors (Mora-Ferrer & Neumeyer, 1996), and the dorsal light reflex through D1- and D2-dopamine receptors (Lin & Yazulla, 1994a). The purpose of this study was to determine whether dopamine influenced movement detection by goldfish, and if so, which dopamine receptor was involved. The D2-dopamine receptor antagonist sulpiride reduced the animal's sensitivity to the moving stimulus, whereas SCH 23390, a D1-dopamine receptor antagonist, did not have any effect. The effect of sulpiride is discussed in relation to known sulpiride effects on retinal neurons and the retinal pigment epithelium.

Absorbance spectra were recorded by microspectrophotometry from 39 different rod and cone types representing amphibians, reptiles, and fishes, with A1- or A2-based visual pigments and λmax ranging from 357 to 620 nm. The purpose was to investigate accuracy limits of putative universal templates for visual pigment absorbance spectra, and if possible to amend the templates to overcome the limitations. It was found that (1) the absorbance spectrum of frog rhodopsin extract very precisely parallels that of rod outer segments from the same individual, with only a slight hypsochromic shift in λmax, hence templates based on extracts are valid for absorbance in situ; (2) a template based on the bovine rhodopsin extract data of Partridge and De Grip (1991) describes the absorbance of amphibian rod outer segments excellently, contrary to recent electrophysiological results; (3) the λmax/λ invariance of spectral shape fails for A1 pigments with small λmax and for A2 pigments with large λmax, but the deviations are systematic and can be readily incorporated into, for example, the Lamb (1995) template. We thus propose modified templates for the main “α-band” of A1 and A2 pigments and show that these describe both absorbance and spectral sensitivities of photoreceptors over the whole range of λmax. Subtraction of the α-band from the full absorbance spectrum leaves a “β-band” described by a λmax-dependent Gaussian. We conclude that the idea of universal templates (one for A1- and one for A2-based visual pigments) remains valid and useful at the present level of accuracy of data on photoreceptor absorbance and sensitivity. The sum of our expressions for the α- and β-band gives a good description for visual pigment spectra with λmax > 350 nm.

We previously showed that immunoreactivity to N-Methyl-D-aspartate (NMDA) receptors in primary visual cortex of Callithrix jacchus is regulated by visual activity during the second and third postnatal months (Fonta et al., 1997). The purpose of the present study was to show that the columnar pattern of high and low NMDAR1 immunoreactivity observed in monocularly deprived animals corresponds to ocular dominance columns linked to the nondeprived and deprived eye, respectively. We compared cortical distribution of NMDAR1 receptors and the projection zones of thalamic afferents, revealed by transneuronal transport of tritiated proline, in 2-month-old, either monocularly deprived or control, marmosets. The data show that ocular dominance columns exist in 2-month-old marmosets and that a 2-week monocular deprivation by means of eyelid suture leads to a modification of the thalamo-cortical afferents organization. Experiments of neuronal tracing and immunohistochemistry performed on the same animals demonstrated that cortical domains with decreased NMDAR1 level correspond to the deprived eye columns. These investigations, coupled to the previous results, strongly suggest that the NMDA receptors, regulated by visual activity, are involved in the refining of ocular dominance columns in the primary visual cortex of juvenile marmoset.

Crayfish photoreceptors exhibit a voltage-dependent potassium conductance, GK, that is generally similar to the delayed rectifier channel described in neurons and other arthropod retinular cells. GK activation (i.e. the apparent threshold, Vth) occurs near the resting potential and GK is substantially reduced by 25 mM extracellular tetraethylammonium (TEA) and by intracellular Cs+ injections. Light exposure, sufficient to reduce visual sensitivity 100-fold, increases Vth (shifts it in the depolarizing direction) by about 20 mV. The light-dependent change in Vth does not depend upon the corresponding increase (depolarization) of the steady-state membrane potential nor does it depend upon inward calcium currents. Vth is slightly influenced by fluctuations in Ko associated with the light-elicited currents. During light exposure Ko (measured with K+-sensitive electrodes) increases by 2.1 mM (equivalent to an 8 mV increase in EK). This increase in EK makes only a modest contribution to the light-dependent change in Vth as determined by perfusion with high potassium salines. Intracellular calcium injections increase Vth by 10 to 20 mV and reduce visual sensitivity by 5- to 10-fold. The results imply that during exposure to high levels of illumination, K+ currents at the steady-state membrane potential are diminished by a calcium-dependent change in GK gating and, to a smaller degree, by a reduced K+ concentration gradient. It is notable that Ca2+ appears to inhibit both GK and the light-elicited conductance from both inside and outside the plasma membrane. As a consequence of the light-dependent change in Vth, GK makes only modest contributions to the changes in sensitivity and speed normally associated with light adaption. These functions are regulated by the transduction pathway and are revealed at the resting potential in the time course and magnitude of the light-elicited currents.

In normal adult cats, a monoclonal antibody directed toward the NR-1 subunit of the N-methyl-d-aspartate (NMDA) receptor (Pharmingen, clone 54.1) produced dense cellular and neuropil labeling throughout all layers of the lateral geniculate nucleus (LGN) and adjacent thalamic nuclei, including the thalamic reticular, perigeniculate, medial intralaminar, and ventral lateral geniculate nuclei. Cellular staining revealed well-defined somata, and in some cases proximal dendrites. NMDAR-1 cell labeling was also evident in the LGN of early postnatal kittens, suggesting that developing LGN cells possess this receptor subunit at or before eye opening. Within the A-layers of the adult LGN, staining encompassed a wide range of soma sizes. Soma size comparisons of NMDAR-1 stained cells with those stained with an antibody directed toward a nonphosphorylated neurofilament protein (SMI-32), which selectively stains Y-relay cells (Bickford et al., 1998), or an antibody to glutamic acid decarboxylase (GAD), which stains for GABAergic interneurons, suggested that NMDA receptors are utilized by relay cells and interneurons. NMDAR-1 staining was also observed in the LGN of cats with early monocular lid suture. Although labeling was apparent in both deprived and nondeprived A-layers of LGN, the distribution of soma sizes was significantly different. In the deprived A-layers of LGN, staining was limited to small- and medium-sized cells. Cells with relatively large soma were lacking. However, cell density measurements as well as soma size comparisons with cells stained for Nissl substance suggested these differences were due to deprivation-induced cell shrinkage and not to a loss of NMDAR-1 staining in Y-cells. Taken together, these results suggest that NMDA receptors are utilized by both relay cells and interneurons in LGN and that alterations in early visual experience do not necessarily affect the expression of NMDA receptors in the LGN.