Amacrine cells are a morphologically and functionally diverse group of inhibitory interneurons. Morphologically, they have been divided into approximately 30 types. Although this diversity is probably important to the fine structure and function of the retinal circuit, the amacrine cells have been more generally divided into two subclasses. Glycinergic narrow-field amacrine cells have dendrites that ramify close to their somas, cross the sublaminae of the inner plexiform layer, and create cross talk between its parallel ON and OFF pathways. GABAergic wide-field amacrine cells have dendrites that stretch long distances from their soma but ramify narrowly within an inner plexiform layer sublamina. These wide-field cells are thought to mediate inhibition within a sublamina and thus within the ON or OFF pathway. The postsynaptic targets of all amacrine cell types include bipolar, ganglion, and other amacrine cells. Almost all amacrine cells use GABA or glycine as their primary neurotransmitter, and their postsynaptic receptor targets include the most common GABAA, GABAC, and glycine subunit receptor configurations. This review addresses the diversity of amacrine cells, the postsynaptic receptors on their target cells in the inner plexiform layer of the retina, and some of the inhibitory mechanisms that arise as a result. When possible, the effects of GABAergic and glycinergic inputs on the visually evoked responses of their postsynaptic targets are discussed.

Mammalian retinae express multiple connexins that mediate the metabolic and electrical coupling of various cell types. In retinal neurons, only connexin36, connexin45, connexin50, and connexin57 have been described so far. Here, we present an analysis of a novel retinal connexin, connexin30.2 (Cx30.2), and its regulation in the mouse retina. To analyze the expression of Cx30.2, we used a transgenic mouse line in which the coding region of Cx30.2 was replaced by lacZ reporter DNA. We detected the lacZ signal in the nuclei of neurons located in the inner nuclear layer and the ganglion cell layer (GCL). In this study, we focused on the GCL and characterized the morphology of the Cx30.2-expressing cells. Using immunocytochemistry and intracellular dye injections, we found six different types of Cx30.2-expressing ganglion cells: one type of ON-OFF, three types of OFF, and two types of ON ganglion cells; among the latter was the RGA1 type. We show that RGA1 cells were heterologously coupled to numerous displaced amacrine cells. Our results suggest that these gap junction channels may be heterotypic, involving Cx30.2 and a connexin yet unidentified in the mouse retina. Gap junction coupling can be modulated by protein kinases, a process that plays a major role in retinal adaptation. Therefore, we studied the protein kinase–induced modulation of coupling between RGA1 and displaced amacrine cells. Our data provide evidence that coupling of RGA1 cells to displaced amacrine cells is mediated by Cx30.2 and that the extent of this coupling is modulated by protein kinase C.

If the relative phase of red and green modulated lights is changed, at low temporal frequencies the response of cells of the magnocellular (MC) pathway has been found to be minimal not to counterphase, chromatic modulation (as expected of a luminance mechanism) but shifted to some phase intermediate between luminance and chromatic modulation. The results could only be modeled by assuming interaction between achromatic and chromatic inputs to MC cells. The ‘phase shift’ resembled that seen with psychophysical threshold measurements using the same stimuli. Psychophysical results also showed that the phase shift is dependent on the chromaticity of a background. The results reported here show that the direction of the phase shift in MC cells is reversed by changing the background from long to short wavelengths and is consistent with psychophysical observations. Cell behavior was again modeled by assuming vector summation of achromatic and chromatic inputs. The reversal of phase-shift direction requires a reversal in polarity of the chromatic input. The underlying physiological mechanism may involve summation of chromatic signals of opposite polarity; if the relative size of these signals depends on the background, this may determine the direction of phase shift.

A DBA/2J (D2) transgenic mouse line with cyan fluorescent protein (CFP) reporter expression in ganglion cells was developed for the analysis of ganglion cells during progressive glaucoma. The Thy1-CFP D2 (CFP-D2) line was created by congenically breeding the D2 line, which develops pigmentary glaucoma, and the Thy1-CFP line, which expresses CFP in ganglion cells. Microsatellite marker analysis of CFP-D2 progeny verified the genetic inclusion of the D2 isa and ipd loci. Specific mutations within these loci lead to dysfunctional melanosomal proteins and glaucomatous phenotype in D2 mice. Polymerase chain reaction analysis confirmed the inclusion of the Thy1-CFP transgene. CFP-fluorescent ganglion cells, 6–20 μm in diameter, were distributed in all retinal regions, CFP processes were throughout the inner plexiform layer, and CFP-fluorescent axons were in the fiber layer and optic nerve head. Immunohistochemistry with antibodies to ganglion cell markers NF-L, NeuN, Brn3a, and SMI32 was used to confirm CFP expression in ganglion cells. Immunohistochemistry with antibodies to amacrine cell markers HPC-1 and ChAT was used to confirm weak CFP expression in cholinergic amacrine cells. CFP-D2 mice developed a glaucomatous phenotype, including iris disease, ganglion cell loss, attrition of the fiber layer, and elevated intraocular pressure. A CFP-D2 transgenic line with CFP-expressing ganglion cells was developed, which has (1) a predominantly D2 genetic background, (2) CFP-expressing ganglion cells, and (3) age-related progressive glaucoma. This line will be of value for experimental studies investigating ganglion cells and their axons in vivo and in vitro during the progressive development of glaucoma.

The morphology of retinal ganglion cells within the central retina during formation of the fovea was examined in retinal explants with horseradish-peroxidase histochemistry. A foveal depression was first apparent in retinal wholemounts at embryonic day 112 (El 12; gestational term is approximately 165 days). At earlier fetal ages, the site of the future fovea was identified by several criteria that included peak density of ganglion cells, lack of blood vessels in the inner retinal layers, arcuate fiber bundles, and the absence of rod outer segments in the photoreceptor layer. Prior to E112, the terminal dendritic arbor of retinal ganglion cells within the central retina extended into the inner plexiform layer and were located directly beneath their somas of origin or at most were slightly displaced from it. For example, at E90 the mean horizontal displacement of the geometric center of the dendritic arbor from the somas of cells within 600 μm of the estimated center of the future fovea was 4.1 μm (S.D. 2.7, range 1.0-10.0, n = 97). Following formation of the foveal depression the dendritic arbors of cells were significantly displaced from their somas. For example, at E138 the mean displacement was 41.2 μm (S.D. 12.2, range 12.0-56.0, n = 97). The displacement of the dendritic arbor which occurred during this period was not accounted for by areal growth of the dendritic arbor, the somas, or the retina, but was produced by the lengthening of the primary dendritic trunk. Moreover, no significant displacement was observed within the remaining 1.5–6.5 mm of the central retina. These observations provide evidence supporting early speculations that the formation of the foveal pit occurs, in part, by the radial migration of ganglion cells from the center of the fovea during its formation. Our analyses suggest that this migration occurs by the lengthening of the primary dendrite presumably by the addition of membrane. This migration is in a direction opposite to the inward movement of photoreceptors that occurs during late fetal and early postnatal periods (Packer et al., 1990, Journal of Comparative Neurology 298, 472–493).

An important mechanism for the discrimination of direction of motion in the retina is a spatially asymmetric inhibition. This inhibition has been postulated to operate either as a subtraction, like in difference-of-Gaussians' models, or as a division, like in shunting-inhibition models of directional selectivity. The latter, but not the former, is nonlinear. This raises the question of whether the inhibitory mechanism involved in directional selectivity is nonlinear. To investigate this issue, we studied the linearity of the contrast dependence of the extracellularly recorded responses to apparent motions in ON-OFF directionally selective ganglion cells of the rabbit retina. The results show that the inhibition underlying directional selectivity is nonlinear and fits shunting-inhibition models well. Other biophysical mechanisms that might account for the type of nonlinearity observed in the data are also considered.

Ganglion cells of the cat retina that are neither alpha nor beta cells are often lumped for convenience into a single anatomical group—the gamma cells (Boycott & Wässle, 1974; Stone, 1983; Wässle & Boycott, 1991). Defined in this way, gamma cells are the morphological counterpart to the physiological W-cell class, which includes all ganglion cells that are neither Y (alpha) nor X (beta) cells. We have estimated the retinal distribution of gamma cells by using retrograde transport to label ganglion cells innervating the superior colliculus and by assuming that these included virtually all gamma cells and no beta cells. We excluded labeled alpha cells on the basis of soma size. Our data suggest that gamma cells represent just under half of the ganglion cells in most of the nasal retina, but only about a third of those in the area centralis and temporal retina. Gamma cells do not appear to be more highly concentrated in the nasal visual streak than are other ganglion cells. In the temporal retina, gamma cells with crossed projections to the brain are apparently at least twice as common as those with uncrossed projections.

The whole-cell configuration of the patch-clamp technique was used to study voltage-gated K+ conductances in retinal ganglion cells from postnatal rat. Retinal ganglion cells were fluorescently labeled in situ, dissociated from the retina, and maintained in culture. With physiological solutions in the bath and the pipette, depolarizing voltage steps from physiological holding potentials activated Na+-(INa), Ca2+ (ICa), and K+ -currents studied previously in retinal ganglion cells. Here we report on a slowly decaying K+ current, not heretofore reported in rat. With 4-AP, TEA, and Co2+ in the bath, to block IA, IK, and IK(Ca), respectively, a slowly decaying outward current was activated from —80 mV by steps positive to —40 mV. This current was present in 92% of all ganglion cells tested (n = 83). It activated within 10 ms and inactivated with a voltage-independent time constant of about 70 ms at 35°C. Inactivation was voltage-dependent, half-maximal at —55 mV, and almost complete at 0 mV. The current was blocked by internal Cs+ and TEA, or by external application of 1 mM Ba2+, but not by 3 mM extracellular Co2+. The biophysical and pharmacological properties of this current are distinctly different from those of slowly inactivating K+ currents studied in other rat neurons. It was very similar, however, to a slowly inactivating K+ current previously reported in ganglion cells of tiger salamander retina. This last finding indicates conservation of a defined K+ channel type in functionally related cells in both lower vertebrates and mammals.

Monoclonal antibodies directed against nicotinic acetylcholine receptors (nAChRs) were used to identify and characterize cholinoceptive neurons in the chick retina. Two monoclonal antibodies (mAbs), mAb 210 and mAb 270, stained many neurons in both the inner nuclear layer (INL) and ganglion cell layer (GCL). A class of large labeled cells in the inner INL were positioned at the INL/IPL (inner plexiform layer) border and resembled displaced ganglion cells (DGCs). Their identity was confirmed with injections of rhodamine-labeled microspheres into the ventral tectum and nucleus of the basal optic root (nBOR). Four days after the injection, large nAChR-positive neurons in the inner INL were labeled with beads. The distribution of these cells matched that reported for DGCs in the chicken and pigeon (Reiner et al., 1979; Fite et al., 1981). Many smaller cells in the INL also exhibited nAChR immunoreactivity. These cells were not retrogradely labeled after bead injections into retinal recipient areas. Their processes entered the IPL where they arborized in a band comprised of the inner leaflet of lamina 1 and all of lamina 2. In some instances, a process continued inward to lamina 4. These neurons were tentatively identified as amacrine cells because of their position and branching pattern.

Approximately 12–18% of the cells in the GCL exhibited nAChR immunoreactivity. Many of these cells could be classified as ganglion cells as their axons were also labeled following exposure to nAChR antibodies. Their distribution mirrored that of all ganglion cells with a higher density of cells in the central retina than in the periphery (Ehrlich, 1981). A “double label” technique was used to compare the distribution of nAChR-positive neurons with that of the choline acetyltransferase-positive (ChAT), cholinergic neurons in the chick retina. The two antigens were visualized with two different fluorophores: FITC and RITC. We were unable to find any cells in either the INL or GCL that exhibited both ChAT- and nAChR-like immunoreactivity. The nAChR-positive cells and the ChAT-positive cells both arborized in two bands within the IPL. The patterns were in perfect register in the inner IPL (lamina 4). But, in the outer IPL, the nAChR-positive dendrites were observed in the inner leaflet of lamina 1 and in all of lamina 2 while the ChAT-positive dendrites did not extend into the innermost portion of lamina 2.

Studies of the numbers of retinal ganglion cells and lateral geniculate nucleus (LGN) neurons in primates suggest that the numbers of both types of neurons may vary over a two-fold range from one individual to another. This raises the question of whether the numbers of ganglion cells and LGN neurons are related or vary independently from individual to individual. We used stereological procedures to obtain unbiased estimates of the numbers of both cell types in seven rhesus monkeys. We found no significant correlation (rs. = −0.21) between the numbers of retinal and LGN cells in the same animals. In agreement with previous studies, the average ratio of the number of retinal ganglion cells that project to the LGN and the number of LGN cells was approximately 1:1. However, this ratio varied over a two-fold range, from 0.78:1 to 1.64:1, in individual animals. These results have important implications for understanding the mechanisms of retino-geniculate development and for understanding the connectional wiring between the retina and LGN.

A large population of amacrine cells in the retina are thought to use GABA as an inhibitory neurotransmitter in their synaptic interactions within the inner plexiform layer. However, little is known about their synaptic targets; the neurons that express the receptors for GABA have not been clearly identified. Recently, the GABAA receptor has been isolated and antibodies have been raised against it. These antibodies have proven useful for the immunocytochemical localization of the receptor, and two brief reports describing the distribution of GABAA receptor immunoreactivity in the retina have appeared (Richards et al., 1987; Mariani et al., 1987). We used a monoclonal antibody (62–3G1) against the GABAA receptor to study the retina of the New World primate Saimiri sciureus.

Labeled somata were found in the inner nuclear layer (INL) and ganglion cell layer (GCL). The staining was confined to what appeared to be the cell's plasmalemma and small cytoplasmic granules. Most of the labeled neurons in the INL had small somata (5–7 μm in diameter) located at the vitreal edge of the layer. They arborized in two laminae (approximately 2 and 4) of inner plexiform layer (IPL). Ventral to the optic disc (2.5 mm) they comprised 29% of the cells present. A few of the labeled neurons appeared to be interplexiform cells or flat bipolar cells, with labeled processes that extended into both the IPL and the inner half of the outer plexiform layer. In the GCL, the labeled somata were among the largest present (13–20 μm in diameter), and 2.5 mm ventral to the optic disc they made up 15% of the cells present. Experiments in which immunoreactive somata were retrogradely labeled following the injection of fluorescent tracers into the optic tract provided a conclusive demonstration that some of the immunoreactive somata were ganglion cells. The antibody often labeled their axons in the optic fiber layer. This suggests that the GABAA receptors are transported anterogradely to the retinal terminal fields. The dendrites of the immunoreactive ganglion cells extended into the 2 laminae of labeled processes in the IPL, and their primary dendritic arbors were, at any given eccentricity, quite similar in appearance. This homogeneity suggests that they comprise a particular subset of the ganglion cells.

Sections simultaneously labeled with the monoclonal antibody against the GABAA receptor and antisera against either L-glutamic acid decarboxylase (GAD) or GABA revealed that the GAD/GABA was distributed much more widely in the IPL than the GABAA receptor. This variance may reflect either the presence of other, perhaps GABAB, receptors in the IPL or GABA in portions of the IPL where it is ineffective as a neurotransmitter.

We investigated whether regenerating mature axons recapitulate embryonic features essential to successful reconnectivity within the injured nervous system. Strips from embryonic and adult chick retinae were cultured, and outgrowing axons were examined morphometrically and immunohistochemically. In addition, the target-recognition properties of adult neurites were analyzed. Regenerating adult axons elongate on a poly-L-lysine/laminin substratum with a speed about one order of magnitude slower than that of embryonic axons. Morphologically, adult axonal tips differ dramatically from embryonic growth cones in that they possess only filopodial extensions whereas embryonic growth cones possess both lamellipodial and filopodial processes. Both embryonic and adult neurites express the growth-associated protein GAP-43. When cultured on alternating stripes of anterior and posterior embryonic tectal membranes, both adult and embryonic retinal axons distinguish between the two membrane preparations. Our results demonstrate that during axonal regeneration the mature neurons express embryonic properties that are involved in the recognition of tectal positional cues.

The entire population of ganglion cells in the retina of the toad Bufo marinus was labeled by retrograde transport of a lysine-fixable biotinylated dextran amine of 3000 molecular weight. Synaptic connections between bipolar, amacrine, and ganglion cells in the inner plexiform layer were quantitatively analyzed, with emphasis on synaptic inputs to labeled ganglion cell dendrites. Synapses onto ganglion cell dendrites comprised 47% of a total of 1234 identified synapses in the inner plexiform layer. Approximately half of the bipolar or amacrine cell synapses were directed onto ganglion cell dendrites, while the rest were made mainly onto amacrine cell dendrites. Most of the synaptic inputs to ganglion cell dendrites derived from amacrine cell dendrites (84%), with the rest from bipolar cell terminals. Synaptic inputs to ganglion cell dendrites were distributed relatively uniformly throughout all sublaminae of the inner plexiform layer. The present study provides unambiguous identification of ganglion cell dendrites including very fine processes, enabling a detailed analysis of the types and distribution of synaptic inputs from the bipolar and amacrine cell to the ganglion cells. The retrograde tracing technique used in the present study will prove to be a useful tool for identifying synaptic inputs to ganglion cell dendrites from neurochemically identified bipolar and amacrine cell types in the retina.

An antiserum directed against tyrosine hydroxylase (TH), the rate-limiting enzyme in the synthesis of dopamine, was used to study the pigeon retina. Labeled cells were observed in both the inner nuclear layer (INL) and ganglion cell layer (GCL). Two populations of TH-immunoreactive neurons were observed in the INL. Some of these cells were 7−10 μ in diameter and gave rise to processes that arborized in three Layers of the inner plexiform layer (IPL). These cells appeared similar to the dopaminergic amacrine cells described previously (Marc, 1988). Other labeled cells in the INL were 12−20 μ in diameter and were recognizable as a previously described subpopulation of TH-immunoreactive displaced ganglion cells (Britto et al., 1988).

A population of labeled cells was observed in the GCL. Counts of these cells in two retinae revealed 5000 and 7000 cells, respectively. They ranged in size from 8−15 μ in diameter in the central retina and from 8−20 m in diameter in the peripheral retina. The density of labeled cells was highest in the central retina and red field and lowest in the retinal periphery. The difference in cell size and cell density as a function of eccentricity is characteristic of the total population of ganglion cells in the avian retina (Ehrlich, 1981; Hayes, 1982). Some of the TH-positive cells in the GCL could be classified as ganglion cells for two reasons: (1) The axons of many of the TH-positive cells in the GCL were TH-immunoreactive as well and could be followed to the optic nerve head. (2) The injection of rhodamine-labeled microspheres into the nucleus geniculatus lateralis, pars ventralis (GLv), resulted in the retrograde labeling of many of the TH-positive cells in the contralateral retina.

Ganglion cells in the albino rat retina were retrogradely labeled with the fluorescent dye, diamidino-yellow, from the superior colliculus. Preembedding and postembedding immunocytochemical techniques were employed in conjunction with computer-assisted image processing to visualize SP- and GABA-immunoreactivity. Examination of flatmount and sectioned retinas revealed that approximately 3% of the ganglion cells projecting to the contralateral superior colliculus exhibit SP-immunoreactivity. Moreover, these cells were found to comprise a subpopulation of the GABA-immunoreactive cells projecting to the rat tectum.

Previous studies have reported that the surround responses of retinal ganglion cells weaken or disappear upon dark adaptation. The mechanism(s) by which this occurs is largely unknown, although changes in activity of retinal dopaminergic neurons have been implicated. In the light-adapted rabbit retina, the surround ON responses of OFF-center ganglion cells have been shown to be markedly reduced or abolished by a dopamine antagonist. This effect of a dopamine antagonist was recently shown to be reversed by the glycine antagonist strychnine and by compounds that elevate intracellular cAMP levels. The present study was conducted to determine whether strychnine and cAMP-elevating compounds could bring out the surround ON responses in OFF-center ganglion cells that are diminished upon dark adaptation. Extracellular recordings of OFF-center brisk ganglion cells were made from isolated, superfused retinal preparations. During the course of dark adaptation, the surround On responses of many cells decreased markedly.Application in both brisk-transient and brisk-sustained OFF-center ganglion cells. The center OFF responses of these cells, on the other hand, were not enhanced by strychnine. Of the cAMP-elevating compounds tested, 8-(4-chlorophenylthio) cyclic AMP was the most effective in bringing out the surround ON responses in dark-adapted OFF-center ganglion cells. The findings from this study suggest that under dark-adapted conditions glycinergic neurons inhibit the surround component of OFF-center ganglion cells. The release of glycine from these neurons is suggested to be regulated by a cAMP-dependent mechanism.

We investigated the role of 5HT3 receptors in the mammalian retina using electrophysiological techniques to monitor ganglion cell activity. Activation of 5HT3 receptors with the selective agonist 1-phenylbiguanide (PBG) increased the ON responses of ON-center ganglion cells, while decreasing the OFF responses of OFF-center cells. The application of a selective 5HT3 antagonist had a reciprocal effect, namely it reduced the center response in ON-center cells and concomitantly increased the center responses in OFF-center cells. Since putative serotoninergic amacrine cells in the retina are connected specifically to the rod bipolar cell, these agents most likely affect the rod bipolar terminal. These data, together with previous studies, suggest that both 5HT2 and 5HT3 receptors mediate an excitatory influence which serves to facilitate the output from rod bipolar cells, the former via a phosphatidyl inositol second-messenger system, and the latter via a direction channel.

The main route of information flow through the vertebrate retina is from the photoreceptors towards the ganglion cells whose axons form the optic nerve. Bipolar cells of the frog have been so far reported to contact mostly amacrine cells and the majority of input to ganglion cells comes from the amacrines. In this study, ganglion cells of frogs from two species (Bufo marinus, Xenopus laevis) were filled retrogradely with horseradish peroxidase. After visualization of the tracer, light-microscopic cross sections showed massive labeling of the somata in the ganglion cell layer as well as their dendrites in the inner plexiform layer. In cross sections, bipolar output and ganglion cell input synapses were counted in the electron microscope. Each synapse was assigned to one of the five equal sublayers (SLs) of the inner plexiform layer. In both species, bipolar cells were most often seen to form their characteristic synaptic dyads with two amacrine cells. In some cases, however, the dyads were directed to one amacrine and one ganglion cell dendrite. This type of synapse was unevenly distributed within the inner plexiform layer with the highest occurrence in SL2 both in Bufo and Xenopus. In addition, SL4 contained also a high number of this type of synapse in Xenopus. In both species, we found no or few bipolar to ganglion cell synapses in the marginal sublayers (SLs 1 and 5). In Xenopus, 22% of the bipolar cell output synapses went onto ganglion cells, whereas in Bufo this was only 10%. We conclude that direct bipolar to ganglion cell information transfer exists also in frogs although its occurrence is not as obvious and regular as in mammals. The characteristic distribution of these synapses, however, suggests that specific type of the bipolar and ganglion cells participate in this process. These contacts may play a role in the formation of simple ganglion cell receptive fields.

Whole-cell voltage clamp in the retinal slice and intracellular current clamp in the intact retina were used to study inhibitory interactions in the inner plexiform layer. Picrotoxin or strychnine reduced inhibitory, light-evoked currents in a majority of ganglion cells. However, in nearly a third of the ganglion cells, each of these antagonists enhanced the inhibitory synaptic current. All inhibitory current was blocked by the addition of the other antagonist. This indicates a cross-inhibition between GABAergic and glycinergic feedforward pathways. Blocking of GABAARs with SR95531 shortened the time course of both excitatory and inhibitory synaptic currents in ganglion cells. Application of picrotoxin, which blocked both GABAARs and GABACRs, produced the opposite effect. Recordings in the intact retina indicated that the light responses of ON bipolar cells, sustained ON, and transient ON-OFF third-order neurons were all made more transient by SR95531 and made more sustained by picrotoxin. The data suggest that a GABAC feedback pathway to bipolar cells makes light responses more phasic and that this feedback is inhibited through a GABAAR pathway. Consequently, the balance between GABAAR and GABACR inhibition regulates the time course of inputs to ganglion cells.

Polyclonal (7493 and 7317) and monoclonal (mAb3) antibodies, generated to the α subunit of the voltage-gated sodium channel (αNaCh), were employed to assess the cell types containing αNaCh-like immunoreactivity in the mature cat and monkey retina. Immunoblot analyses of retinal proteins in the cat revealed that the polyclonal and monoclonal antibodies we employed labeled a band in the 260–kDa region which corresponds to the molecular mass of the α subunit of the NaCh. In both the cat and monkey, these antibodies immunolabeled several distinct types of retinal cells. With the polyclonal antibodies immunoreactivity was observed in ganglion cells and their intraretinal axons, in horizontal cells, and unexpectedly, in cones. In addition, in both species, a limited number of heavily labeled profiles, presumed to be bipolar cells, were seen in the inner nuclear layer. In cat and monkey the monoclonal antibody labeled axons in the fiber layer, ganglion cell somata, and a continuous band of immunoreactive cell bodies (presumed bipolar cells) situated in the outer half of the inner nuclear layer. By immunolabeling isolated cells dissociated from the cat retina, it was possible to demonstrate unequivocally that a population of bipolar cells was labeled by the monoclonal and the polyclonal antibodies we employed. The differences in the labeling observed with the monoclonal antibody as compared to the polyclonal antibodies were interpreted as reflecting the presence of different α-subunit subtypes in the mammalian retina. Collectively, our findings suggest that αNaCh-like proteins are expressed by a more diverse population of retinal cells than expected on the basis of previous physiological and immunohistochemical studies.