Ionotropic glutamate receptors in isolated horizontal cells of the rabbit retina

With the use of the whole-cell voltage-clamp technique, we have recorded the currents induced by ionotropic glutamate receptor agonists on isolated axonless horizontal cells (HC) of rabbit retina. Bath application of the non-N-methyl-D-aspartate receptor agonists: kainate (KA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and L-glutamate (GLU) produced an increase in the conductance for non-selective cations. All the isolated horizontal cells responded to GLU, AMPA and KA. Responses elicited by GLU and AMPA but not KA exhibited a concentration-dependent desensitization. Application of N-methyl-D-aspartate (NMDA) evoked no responses. The rank order affinities of the agonists as estimated from EC50 values were AMPA > GLU > KA. Whereas KA had the lowest affinity of the agonists tested, it produced the largest currents. Hill coefficients of the concentration-response data were near 1 for AMPA, and 2 for KA and GLU. Coapplication of AMPA with cyclothiazide (CTZ) blocks AMPA receptor desensitization, and enhanced its effects on conductance. However, CTZ did not change the KA -induced conductances. In all cells tested, 6,7-dinitroquinoxaline (DNQX) completely and reversibly blocked the effects of KA and AMPA. The KA- and AMPA-induced currents were also completely blocked by 1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine (GYKI 52466), a selective AMPA receptor antagonist. These results indicate that the responses to glutamate agonists in HC were mediated almost exclusively by AMPA receptors. Our study indicates that AMPA receptors play a fundamental role in mediating the synaptic input into rabbit horizontal cells.     

Stimulation of photoreceptor disc shedding and pigment epithelial phagocytosis by glutamate,aspartate, and other amino acids

It has been reported that aspartate and glutamate selectively impair the structure (Olney, '82) and function (e.g., Furakawa and Hanawa, '55) of second- and third-order retinal neurons while leaving the photoreceptor unaffected. Either amino acid may mimic the endogenous photoreceptor neurotransmitter (Ehinger, '82). We report here that excitatory amino acids also induce massive rod photoreceptor disc shedding in eyecups of Xenopus laevis maintanined in vitro. Disc shedding is the process whereby photoreceptors eliminate effete discs. It involves interaction between the distal outer segment and pigment epithelium. Millimolar L-asparate and L-glutamate, as well as micromolar kainic acid, a glutamate analog, stimulate disc shedding three-to fivefold higher than normal light-evoked shedding levels and result in extensive inner retinal damage. Fifty-millimolar KC1, 1.0 μM ouabain, and replacement of sodium with choline also stimulate disc shedding and alter retinal structure. Extensive neurotoxicity appears unrelated to disc shedding since other amino acids having no significant or marginal effects on retinal structure also stimulate shedding. While the site and mechanism of action of these effectors, and in particular the excitatory amino acids, is now undefined, the data show that amino acids thought to act directly and specifically on inner retinal neurons can also markedly alter photoreceptor and pigment epithelial metabolism.     

Effects of excitatory amino acids,and of their agonists and antagonists on the release of neurotransmitters from the chick retina

Effects of glutamic, aspartic, and cysteic acid, and of kainic acid and N-methyl aspartate on the release of labeled GABA, glycine, and taurine were examined in isolated, perfused chick retina. Glutamic acid (0.5-2 mM), increased the release of ³H-GABA by more than four times and that of ¹⁴C-glycine by about two times. The release of GABA decreased 50% and that of glycine 95% in the presence of the antagonist of glutamic acid receptors, glutamate diethyl ester (300 m?M). N-methyl aspartate, used as an agonist of aspartic acid receptors, preferentially increased the release of GABA (seven times) over that of glycine (three times). The stimulatory effect of N-methyl aspartate was antagonized by D-α aminoadipate and by Mg. Kainic acid (10 m?M) induced the release of glycine but not that of GABA. Cysteic acid failed to modify the release of any of the amino acids examined. The efflux of labeled taurine was practically unaffected by all the compounds utilized. The release of GABA by the excitatory amino acids and agonists was Ca-independent but Na-dependent, whereas the release of glycine was markedly Ca-dependent. The evidence presented here suggests that experimental conditions activating receptors of excitatory amino acids differently affect the release of inhibitory amino acids.     

N-methyld-aspartate acts as an antagonist of the photoreceptor transmitter in the carp retina

Glutamate, aspartate, and their agonists, kainate, quisqualate, cysteine sulfinate and N-methyl-d-aspartate (NMDA), were applied to the isolated carp retina while recording from horizontal cells. All these agents, except NMDA, depolarized horizontal cells membrane and reduced responses to light, thus mimicking the effect of the endogenous photorecepto transmitter. Application of NMDA, on the other hand, caused a membrane hyperpolarization of horizontal cells in the dark, an effect different from its depolarizing effect as observed elsewhere in the central nervous system. NMDA also reduced or blocked the light responses of these cells as well as the depolarizing responses to applications of glutamate, aspartate or kainate. Effects of NMDA on the spectral properties of the horizontal cell responses were identical to the effects of the acidic amino acid receptor antagonists α-methyl glutamate, and α-amino adipate. Thus, NMDA appears to act as a weak antagonist to the photoreceptor transmitter, whose receptors on the horizontal cell membrane interact with a glutamate-like substance but appear atypical of glutamate receptors described elsewhere in the brain.     

Rod and cone input to horizontal cells in the rabbit retina

In the rabbit retina, there are two types of horizontal cell (HC). The A-type HC is axonless and extensively coupled. The B-type HC is axon bearing; the somatic dendrites are radially symmetric and form a second coupled network, while the axon branches expansively to form a complex terminal structure. The B-type axon terminals (ATs) are independently coupled to form a third network in the outer plexiform layer. We have modified our dye-injection methods to obtain detailed fills of the three different horizontal cell networks for analysis via confocal microscopy. We have confirmed that A-type HCs and the somatic dendrites of B-type HCs receive input exclusively from cones, whereas the B-type ATs receive input only from rods. A single B-type AT may receive input from as many as 1,000 rods, but, surprisingly, our data reveal only one end terminal per rod spherule. The somatic dendrites of A- and B-type HCs form clusters at each cone pedicle coincident with GluR2/3 and GluR4 glutamate receptor subunits. The B-type ATs have GluR2/3- or GluR4-labeled glutamate receptors in two locations: small puncta on the end terminals within the rod spherule invagination and large clusters on the terminal stalks, approximately 1.5 microm from the rod synaptic ribbon. We conclude that AMPA receptors of the same or similar composition mediate photoreceptor input to all types of HCs.     

Distribution of two splice variants of the glutamate transporter GLT1 in the retinas of humans, monkeys, rabbits, rats, cats, and chickens

Antibodies have been generated against two carboxyl-terminal splice variants of the glutamate transporter GLT1, namely, the originally described version of GLT1 and GLT1-B, and labelling has been examined in multiple species, including chickens and humans. Although strong specific labelling was observed in each species, divergent patterns of expression were noted. Moreover, each antibody was sensitive to the phosphorylation state of the appropriate protein, because chemical removal of phosphates using alkaline phosphatase revealed a broader range of labelled elements in most cases. In general, GLT1-B was present in cone photoreceptors and in rod and cone bipolar cells in the retinas of rabbits, rats, and cats. In the cone-dominated retinas of chickens and in marmosets, GLT1-B was associated only with cone photoreceptors, whereas, in macaque and human retinas, GLT1-B was associated with bipolar cells and terminals of photoreceptors. In some species, such as cats, GLT-B was also present in horizontal cells. By contrast, GLT1 distribution varied. GLT1 was associated with amacrine cells in chickens, rats, cats, and rabbits and with bipolar cells in marmosets and macaques. In the rat retina, rod photoreceptor terminals also contained GLT1, but this was evident only in enzymatically dephosphorylated tissues. We conclude that the two variants of GLT1 are present in all species examined but are differentially distributed in a species-specific manner. Moreover, each cell type generally expresses only one splice variant of GLT1.     

Effect of selective kainate lesions on the release of glutamate and aspartate from chick retina

In order to contribute evidence leading to establishing the excitatory pathways in the vertebrate retina, we selectively lesioned chick retinas by intraocular injection of 6, 60, 120, and 200 nmol of kainate, which selectively damages OFF-bipolars, amacrines, horizontals, and ON-bipolars, and measured the K+-stimulated, Ca++-dependent release of L-(3H)-glutamate and L-(3H)-aspartate. We also measured (3H)-GABA release as a marker for horizontal cells and a population of amacrines, as well as (14C)-glycine release as a tracer of a different subpopulation of amacrines. All four amino acids were released from control retinas by a depolarizing K+ concentration in a Ca++-dependent fashion. GABA and glycine, however, showed an additional Ca++-independent component of release. Lesion induced by 6 nmol of kainate decreased by 50% the release of glutamate and by 20% that of aspartate; glycine release was reduced 40% while GABA release was unaffected. Injection of 60 nmol of kainate reduced glutamate release a further 20% and significantly decreased GABA (50%) and glycine (75%) release; aspartate release remained unmodified; 120 nmol of kainate caused a further 30% reduction in aspartate and GABA release. Neither compound was significantly released after treatment with 200 nmol of kainate. These results seem to suggest that while OFF-bipolars could release glutamate as transmitter, aspartate is released from a different cell population which is less sensitive to kainate, probably ON-bipolars.     

Intracellular acidification of the leech giant glial cell evoked by glutamate and aspartate

Glutamate is an excitatory receptor agonist in both neurones and glial cells, and, in addition, glutamate is also a substrate for glutamate transporter in glial cells. We have measured intracellular and extracellular pH changes induced by bath application of glutamate, its receptor agonist kainate, and its transporter agonist aspartate, in the giant neuropile glial cell in the central nervous system of the leech Hirudo medicinalis, using double-barrelled pH-sensitive microelectrodes. The giant glial cells responded to glutamate and aspartate (100–500 μM), and kainate (5–20 μM) with a membrane depolarization or an inward current, and with a distinct intracellular acidification. Glutamate and aspartate (both 500 μM) evoked a decrease in intracellular pH (pH_i) by 0.187 ± 0.081 (n = 88) and 0.198 ± 0.067 (n = 86) pH units, respectively. With a resting pH_i of 7.1 or 80 nM H⁺, these acidifications correspond to a mean increase of the intracellular H⁺ activity by 42 nM and 45 nM. Kainate caused a decrease of pH_i by 0.1 − 0.35 pH units (n = 15). The glutamate/aspartate-induced decrease in pH_i was not significantly affected by the glutamate receptor blockers kynurenic acid (1 mM) and 6-cyano-7-dinitroquinoxaline-2,3-dione (CNQX, 50–100 μM), which greatly reduced the kainate-induced change in pH_i. Extracellular alkalinizations produced by glutamate and aspartate were not affected by CNQX. Reduction of the external Na⁺ concentration gradually decreased the intracellular pH change induced by glutamate/aspartate, indicating half maximal activation of the acidifying process at 5–10 mM external Na⁺ concentration. When all external Na⁺ was replaced by NMDG⁺, the pH_iresponses were completely suppressed (glutamate) or reduced to 10% (aspartate). When Na⁺ was replaced by Li⁺, the glutamate- and aspartate-evoked pH_i responses were reduced to 18% and 14%, respectively. Removal of external Ca²⁺ reduced the glutamate- and aspartate-induced pH_i responses to 93 and 72%, respectively. The glutamate/aspartate-induced intracellular acidifications were not affected by the putative glutamate uptake inhibitor amino-adipidic acid (1 mM). DL-aspartate-β-hydroxamate (1 mM), and dihydrokainate (2 mM), which caused some pH_i decrease on its own, reduced the glutamate/aspartate-induced pH_i responses by 40 and 69%, respectively. The putative uptake inhibitor DL-threo-β-hydroxyaspartate (THA, 1 mM) induced a prominent intracellular acidification (0.36 ± 0.05 pH units, n = 9), and the pH_i change evoked by glutamate or aspartate in the presence of THA was reduced to less than 10%. The results indicate that glutamate, aspartate, and kainate produce substantial intracellular acidifications, which are mediated by at least two independent mechanisms: 1) via activation of non-NMDA glutamate receptors and 2) via uptake of the excitatory amino acids into the leech glial cell. © 1997 Wiley-Liss Inc.     

Anatomical evidence for glutamate and/or aspartate as neurotransmitters in the geniculo-, claustro-, and cortico-cortical pathways to the cat striate cortex

Data obtained by using various experimental approaches suggest that in the mammalian brain, most neurons within the visual system projecting to the striate cortex employ excitatory amino acids as transmitters. In order to investigate further the neurotransmitter phenotype of the ipsilateral afferents to area 17 of the cat, we have injected D-[³H]-aspartate, a retrograde tracer which selectively reveals putative glutamatergic and/or aspartatergic pathways, into this area. Retrogradely labelled neurons were observed in the dorsal lateral geniculate nucleus, visual claustrum, cortical areas 18, 19, 21a, and in both posteromedial and posterolateral parts of the suprasylvian areas but not in other known thalamic afferents such as the lateral posterior-pulvinar complex and the intralaminar nuclei. The distribution and localization of the labelled cells in all these regions were similar to that observed by using the non-selective tracer horseradish peroxidase conjugated to wheat germ agglutinin, though the number of cells was higher with the latter. Our findings provide additional evidence for the presence of excitatory amino acids as neurotransmitters in the major afferents to the cat striate cortex. © 1996 Wiley-Liss, Inc.     

Signals from cone photoreceptors to L-type horizontal cells are differentially modulated by low calcium in carp retina

Ca2+ plays crucial roles in both phototransduction and calcium-dependent glutamate release from the photoreceptor terminal. Modulation, by lowering extracellular Ca2+, of red-sensitive (R-) and short wavelength-sensitive (S-) cone-driven light responses of L-type horizontal cells (LHCs) was studied in the isolated superfused carp retina using intracellular recording techniques. Low Ca2+ (nominally Ca2+-free) Ringer's reduced responses of LHCs to both green (500 nm) and red (680 nm) flashes in darkness, with the former being suppressed more substantially than the latter. This differential suppression became more significant when contribution of R-cones to the green-light-induced responses was diminished by a moderate red (680 nm) background light. Application of IBMX, an inhibitor of phosphodiesterase (PDE), increased LHC responses to both red and green flashes equally, resembling the effect of low Ca2+ on phototransduction. In addition, photopic electroretinographic P III responses, reflecting the activity of cones, to red flashes were more potentiated by low Ca2+, compared to those to green flashes, whilst they were both equally potentiated by IBMX. Furthermore, low Ca2+ caused a more pronounced suppression of LHC responses to red flashes than those to green flashes in the presence of IBMX. It is postulated that reduction of LHC responses in low Ca2+ may be due to the 'saturation suppression' caused by the increased glutamate release from the photoreceptor terminal and the differential modulation may reflect a consequence of the dual action of low Ca2+ on the PDE activity in the photoreceptor outer segment and the synaptic strength between cones and LHCs.     

Dual effect of glutamate and aspartate on the on-center bipolar cell in the carp retina

In on-center bipolar cells of the carp retina, glutamate and aspartate applied extracellularly by pressure injection produced hyperpolarizing potential changes. These responses were not blocked by Co²⁺. Examination of reversal potentials revealed two different conductance changes. One of them appears to be an increase in K⁺ and/or Cl⁻ conductance and other a decrease in Na⁺ conductance. The results are discussed with relation to the difference in ionic mechanisms of cone and rod inputs.     

Uptake and release of neurotransmitter candidates, [3H]serotonin, [3H]glutamate,and [3H]γ-aminobutyric acid,in taste buds of the mudpuppy,Necturus maculosus

Neurotransmitters in vertebrate taste buds have not yet been identified with confidence. Serotonin, glutamate, and γ-aminobutyric acid (GABA) have been postulated, but the evidence is incomplete. We undertook an autoradiographic study of [³H]serotonin, [³H]glutamate, and [³H]GABA uptake in lingual epithelium from the amphibian, Necturus maculosus, to determine whether taste bud cells would accumulate and release these substances. Lingual epithelium containing taste buds was incubated in low concentrations (0.4–6 μM) of these tritiated transmitter candidates and the tissue was processed for light microscopic autoradiography. Merkel-like basal taste cells accumulated [³H]serotonin. When the tissue was treated with 40 mM K⁺ after incubating the tissue in [³H]serotonin, cells released the radiolabelled transmitter. Furthermore, depolarization (KCl)-induced release of [³H]serotonin was Ca-dependent: if Ca²⁺ was reduced to 0.4 mM and 20 mM Mg²⁺ added to the high K⁺ bathing solution, Merkel-like basal cells did not release [³H]serotonin. In contrast, [³H]glutamate was taken up by several cell types, including non-sensory epithelial cells, Schwann cells, and some taste bud cells. [³H]glutamate was not released by depolarizing the tissue with 40 mM K⁺. [³H]GABA uptake was also widespread, but did not occur in taste bud cells. [³H]GABA accumulated in non-sensory epithelial cells and Schwann cells. These data support the hypothesis that serotonin is a neurotransmitter or neuromodulator released by Merkel-like basal cells in Necturus taste buds. The data do not support (nor rule out) a neurotransmitter role for glutamate or GABA in taste buds. J. Comp. Neurol. 392:199–208, 1998. © 1998 Wiley-Liss, Inc.     

Immunocytochemical localization of three vesicular glutamate transporters in the cat retina

Vesicular transporters play an essential role in the packaging of glutamate for synaptic release and so are of particular importance in the retina, where glutamate serves as the neurotransmitter for photoreceptors, bipolar cells, and ganglion cells. In the present study, we have examined the distribution of the three known isoforms of vesicular glutamate transporter (VGLUT) in the cat retina. VGLUT1 was localized to all photoreceptor and bipolar cells, whereas VGLUT2 was found in ganglion cells. This basic pattern of complementary distribution for the two transporters among known populations of glutamatergic cells is similar to previous findings in the brain and spinal cord. However, the axon terminals of S-cone photoreceptors were found to express both VGLUT1 and VGLUT2 and some ganglion cells labeled for both VGLUT2 and VGLUT3. Such colocalizations suggest the existence of dual modes of regulation of vesicular glutamate transport in these neurons. Staining for VGLUT2 was also present in a small number of varicose processes, which were seen to ramify throughout the inner plexiform layer. These fibers may represent axon collaterals of ganglion cells. The most prominent site of VGLUT3 immunoreactivity was in a population of amacrine cells; the axon terminals of B-type horizontal cells were also labeled at their contacts with rod spherules. The presence of the VGLUT3 transporter at sites not otherwise implicated in glutamate release may indicate novel modes of glutamate signaling or additional roles for the transporter molecule.     

Neuropharmacological actions of kynurenic and quinolinic acids on horizontal cells of the isolated fish retina

We have studied the effects of naturally occurring metabolites of tryptophan, kynurenic and quinolinic acids, on the electrophysiological responses of retinal horizontal cells in the fish (Rutilus rutilus, the roach). Quinolinic acid usually hyperpolarizes the cells and reduces their light evoked responses (S-potentials) but on occasion, it causes a slight depolarization of the membrane potential. These actions are similar to those found with N-methyl-d-aspartate (NMDA) and our results are consistent with the proposal that it acts at NMDA binding sites. Kynurenic acid (1mM) invariably hyperpolarizes horizontal cells to their potassium Nernst equilibrium potential and, more significantly, blocks the depolarizing actions exerted on them by excitatory amino acids, such as kainic and quisqualic acids. We show that this action persists in the presence of the synaptic blocker, cobalt chloride, and thus is not mediated by chemical synaptic activity. Kynurenic acid does not reverse depolarization of horizontal cells by dopamine or γ-aminobutyric acid, thus its inhibitory effects are selective to the actions of excitatory amino acids. Neither xanthurenic acid, a close structural analogue of kynurenic acid, nor quinolinic acid are effective in blocking depolarizations by excitatory aino acids.     

Effects of glutamic acid and related agents on horizontal cells in a marine teleost retina

Excitatory amino acids (EAAs) such as glutamic and aspartic acids, considered as the most likely neurotransmitters at the photoreceptor-horizontal cell synapse of teleost retinas, as well as agonists such as kainic acid and several of their antagonists, were applied to isolated and superfused retinas of the teleost Eugerres plumieri. Intracellular recordings from horizontal cells reveal that EAA receptors are of the kainate-quisqualate type. There is competitive inhibition between the agonist and anatogonist agents used, and under their combined effect, the synapse under study remains operational, in a functional state, able to modulate the horizontal cell membrane potential upon retinal illumination. © 1996 Wiley-Liss, Inc.     

Connexin 57 is expressed by the axon terminal network of B-type horizontal cells in the rabbit retina

In the rabbit retina there are two types of horizontal cell (HC). A-type HCs (AHC) are axonless and extensively coupled via connexin (Cx)50 gap junctions. The B-type HC (BHC) is axon-bearing; the somatic dendrites form a second network coupled by gap junctions while the axon terminals (ATs) form a third independent network in the outer plexiform layer (OPL). The mouse retina has only one type of HC, which is morphologically similar to the B-type HC of the rabbit. Previous work suggested that mouse HCs express Cx57 (Hombach et al. [2004] Eur J Neurosci 19:2633-2640). Therefore, we cloned rabbit Cx57 and raised an antibody to determine the distribution of Cx57 gap junctions among rabbit HCs. Dye injection methods were used to obtain detailed fills for all three HC networks for analysis by confocal microscopy. We found that Cx57 was associated with the B-type AT plexus. Cx57 plaques were anticorrelated with the B-type somatic dendrites and the A-type HC network. Furthermore, there was no colocalization between Cx50 and Cx57. We conclude that in the rabbit retina, Cx57 is only found on BHC-AT processes. Thus, in species where there are two types of HC, different connexins are expressed. The absence of Cx57 labeling in the somatic dendrites of B-type HCs suggests the possibility of an additional unidentified HC connexin in the rabbit.     

Stimulation of GABA release from retinal horizontal cells by potassium and acidic amino acid agonists

The release of [³H]GABA from horizontal cells of goldfish retina was studied by biochemical analysis of perfused isolated retina. Retinas were incubated for 15 min in 0.72 μM[³H]GABA, rinsed for 30 min and then perfused with 1 min pulses of increasing concentrations of K⁺ and acidic amino acid agonists under a variety of conditions. Radioactivity in the perfusate was determined by liquid scintillation spectroscopy. The main findings are: (1) virtually all of the [³H]GABA released byl-glutamate (l-Glu) andl-aspartate (l-Asp) and 50% of the K⁺-evoked release, is calcium independent; (2) K⁺-evoked [³H]GABA release is only 10% of that released byl-Glu; (3) threshold [³H]GABA release occurs with 320 μMl-Glu, 1175 μMl-Asp, 4μM quisqualic acid (QA), 4μM kainic acid (KA) and 53 μM N-methyl-dl-aspartate (NMDLA); (4) the quisqualate antagonist glutamic acid diethyl ester (GDEE), has no specific inhibitory action on any of the agonists, whereasd-α-aminoadipic acid (DαAA), an NMDA antagonist, potently inhibits the action of NMDLA andl-Asp; (5) the presence of Mg²⁺, even at 1 mM, totally inhibits NMDLA and also inhibits the action ofl-Glu andl-Asp below 1 mM; (6)d-Asp potentiates the action ofl-Glu by 0.6–0.8 log units and completely inhibits the action ofl-Asp; (7)l-Asp at a ratio of 3:1 potentiates the effect ofl-Glu. From these and other results one concludes that: (a) [³H]GABA release from H1 cells is calcium independent and depends on factors other than passive depolarization, probably sodium; (2) the likely transmitter of red cones isl-Glu acting on quisqualate or kainate receptors, and (3)l-Asp acts predominantly on NMDA receptors and may provide a modulatory role in the outer retina by potentiating the action ofl-Glu.     

Morphological types and connectivity of horizontal cells found in the adult zebrafish (Danio rerio) retina

We describe here different types of horizontal cells in the zebrafish retina and how they connect to photoreceptors. To label horizontal cells, crystals of DiI were placed onto the tips of pulled glass pipettes and inserted into the inner nuclear layer of fixed whole-mount retinas. The DiI-labeled horizontal cells were imaged by confocal microscopy and analyzed according to dendritic arborization, cell depth, dendritic terminal morphology, and connectivity with photoreceptors. Three types of horizontal cells were unequivocally identified: two cone-connecting (H1/2 and H3) and one rod-related cell. H1/2 cells have dendritic terminals that are arranged in "rosette" clusters and that connect to cone photoreceptors without any apparent specificity. H3 cells are larger and have dendritic terminal doublets arranged in a rectilinear pattern. This pattern corresponds to the mosaic of the single cones in the zebrafish photoreceptor mosaic and indicates that H3 cells connect specifically to either the blue-sensitive (long-single) or ultraviolet-sensitive (short-single) cones. Thus, H3 cells are likely to be chromaticity-type cells that process specific color information, whereas H1/2 cells are probably luminosity-type cells that process luminance information. Rod horizontal cells were identified by their shape and dendritic pattern, and they connect with numerous rod photoreceptors via small spherical terminals.     

The role of the retinal interplexiform cell: effects of 6-hydroxydopamine on the spatial properties of carp horizontal cells

The spatial properties of carp horizontal cells were studied after intraocular injection of 6-hydroxydopamine (6-OHDA). This treatment has been shown to destroy dopaminergic nerve terminals as well as decrease dopamine levels in the carp retina. The receptive field size of horizontal cells from retinas treated with 6-OHDA were found to be larger than those from control retinas.     

Spatial orientation of horizontal cell axon terminals in the carp retina

In flatmounts of the carp (Cyprinus carpio) retina, 646 horizontal cells were singly marked by intracellular Lucifer yellow CH (LY) in the presence of dopamine or amphetamine, agents which were useful for restricting LY to single injected cells. Most axon terminals of cone-connected horizontal cells have a tendency to orient either radially or tangentially in the retinal field with respect to the optic disc as a center. Although the fluorescent cellular (dendritic field) area greatly varied depending upon the cell type (L-, RG- and YRB-type), the lengths of the axonal processes (axon plus terminal) were all comparable (400-600 microns). A few cells (4.1% of cells with visible axons) possessed a bifurcate axon with two axon terminals. Axons were not observed on rod-connected horizontal cells. The cellular area and the axonal length of L- and RG-type cells appeared to be smaller in the central than in the intermediate region of the retinal field.