Localization of L-glutamic acid decarboxylase mRNA in monkey and human retina by in situ hybridization

Immunocytochemical studies with gamma-aminobutyric acid (GABA) antibodies and glutamic acid decarboxylase antibodies have shown that the primate retina contains GABAergic amacrine, interplexiform, and displaced amacrine cells. In addition, subpopulations of photoreceptors and horizontal cells have also been suggested to be GABAergic in this retina. In the present study, we have used in situ hybridization to localize GABAergic neurons in human and monkey retinas. In situ hybridizations were carried out with 35S-labeled DNA and RNA probes derived from human and cat glutamic acid decarboxylase cDNA clones. In the monkey retina, labeled cells were present in the inner nuclear and ganglion cells layers. The outer nuclear layer or the inner segment layer had only background levels of labeling. In the inner nuclear layer, all labeled somata were located in the vitread-half bordering the inner nuclear layer/inner plexiform layer boundary. These cells constituted approximately 83% of all labeled cells. Labeled cells were also seen in the ganglion cell layer. In the human retina, labeled somata were observed only in the inner nuclear and the ganglion cell layers. In the inner nuclear layer, the majority of labeled cells were located close to the inner nuclear layer/inner plexiform layer boundary although a minor population of labeled somata (approximately 20%) were found deeper in the inner nuclear layer. The distribution of glutamic acid decarboxylase mRNA-containing cells we observed is in good agreement with the known location of GABAergic neurons. We, however, did not find glutamic acid decarboxylase mRNA in either horizontal cells or photoreceptors in monkey and human retina.     

Colocalization of GAD-like immunoreactivity and 3H-GABA uptake in amacrine cells of rabbit retina

Rabbit retinas were double labeled to determine the degree of colocalization of glutamic-acid-decarboxylase-like immunoreactivity (GAD-like IR) and 3H-GABA uptake using light (LM) and electron microscopic (EM) autoradiography. Both GAD-like IR and 3H-GABA uptake were found in amacrine cell bodies in the inner nuclear layer (INL) as well as in cell bodies in the ganglion cell layer (GCL), and throughout the inner plexiform layer. GAD-like IR was found in 32% of the amacrine cells in the INL, 86% of which also showed 3H-GABA uptake; 3H-GABA uptake was observed in 38% of the amacrine cells. However, only 72% of these cells showed GAD-like IR. Labeled cells in the GCL were only 10-15% as common as similarly labeled cells in the INL. As in the INL, all GAD-positive cells in the GCL were double labeled, but only 53% of the cells taking up 3H-GABA were double labeled. We suggest that labeled cells in the GCL were ganglion cells rather than displaced amacrine cells. Cells, in both the INL and GCL, that showed 3H-GABA uptake but no GAD-like IR had a higher average grain density than double-labeled cells, indicating that uptake by these cells was specific. The relevance to GABAergic function of 3H-GABA uptake without an indication of GAD-like IR is yet to be determined. Statistical analysis at the EM level showed that one-third of the GAD-positive synaptic terminals of amacrine cells were double labeled after a 4-month exposure. Longer exposures at the EM level should reveal a higher percentage of GAD-positive terminals because at the LM level, one-half of the double-labeled cell bodies were "lightly" labeled with grains. The high degree of colocalization of GAD-like IR and 3H-GABA uptake suggests that both markers may be useful for labeling GABAergic neurons in the rabbit retina.     

Localization of G protein-coupled receptor kinases (GRKs) in the avian retina

G protein-coupled receptor kinases (GRKs) are enzymes involved in agonist-dependent regulation of G protein-coupled receptors. In the present work, we characterized, by immunohistochemistry, the presence of GRKs 2, 3 and 5 in the chick retina, a tissue whose structure and neurochemistry are well known. These enzymes are expressed in specific cell types and regions of the retina. Immunoreactivity for GRK2 was found over photoreceptor inner segments, cell bodies of horizontal, amacrine and ganglion cells. Labeling for this enzyme was also observed over the two plexiform layers. Immunoreactivity for GRK3 was found in cell bodies of amacrine and ganglion cells. In plexiform layers, specific GRK3 immunoreactivity was observed only at the inner plexiform layer, where three bands of high labeling were detected. In contrast to GRK2 and 3, intense immunoreactivity for GRK5 was observed only over Müller cells. Occasionally, labeled amacrine cell bodies were also observed. These results suggest that GRKs 2, 3 and 5 are expressed and involved in the physiology of specific cells types of the retina. They also suggest that receptor-GRK specificity may be determined by the co-expression of the receptor and the kinase within individual cell populations in this tissue.     

Cellular localization of N-acetylaspartylglutamate in amphibian retina and spinal sensory ganglia

Antisera were produced against N-acetylaspartylglutamate (NAAG) and were used to localize the molecule within the retina and spinal sensory ganglia of Rana pipiens. NAAG immunoreactivity (IR) in the retina was confined to a subpopulation of amacrine and bipolar cells. The dipeptide was present in the perikarya of these cells and their neurites which terminated in two discrete bands of the inner plexiform layer. Some NAAG-IR was also present in the outer plexiform layer and the inner segment layer. In spinal ganglia, a subpopulation of relatively large sensory neuron cell bodies expressed NAAG-IR. These data are consistent with the hypothesis that this dipeptide has a function which is specific to discrete subclasses of neurons. In the amphibian retina, the NAAG distribution can be related to the reported involvement of the N-methyl-D-aspartate receptor in neurotransmission at the level of amacrine and ganglion cells.     

Light microscopic localization of putative glycinergic neurons in the larval tiger salamander retina by immunocytochemical and autoradiographical methods

Putative glycinergic neurons in the larval tiger salamander retina were localized by a comparative analysis of high affinity 3H-glycine uptake and glycine-like immunoreactivity (Gly-IR) at the light microscopic level. Commonly labeled neurons include at least three types of amacrine cell (Type IAd, Type IAb, Type IIAd; distinguished by soma location and dendritic ramification), cell bodies in the ganglion cell layer (GCL), and rarely observed Type II (inner) bipolar cells. With the increased resolution provided by Gly-IR, we identified a Type IAa amacrine cell, two types of Type IIAd amacrine cells, and Gly-IR interplexiform cells. Gly-IR axons in longitudinal sections of the optic nerve indicate the presence of Gly-IR ganglion cells. The percentage of labeled somas in the inner nuclear layer (INL) compared to all cells in each layer was similar for the two methods: 30-40% in INL 2 (middle layer of somas), 30-40% in INL 3 (inner layer of somas), and about 5% in the GCL. Labeled processes were found throughout the full thickness of the inner plexiform layer (IPL), but with a much denser band in the proximal half (sublamina b). The only major difference between the two methods (3H-glycine uptake vs. Gly-IR) was that Type I (outer) bipolar cells were labeled only by 3H-glycine uptake; these cells were more lightly labeled with silver grains than cell bodies in either INL 2 or INL 3. Postembed labeling of 1 micron Durcupan plastic sections for Gly-IR showed the same pattern, but with much higher resolution, as obtained with 10 micron cryostat sections. This study indicates extensive colocalization of labeling by both probes in INL 2, INL 3, the IPL, and the GCL. We conclude that Gly-IR can serve as a valid and reliable marker for glycine-containing neurons in this retina and suggest that glycine serves as a transmitter for several morphologically distinct types of amacrine cell, an interplexiform cell, and perhaps a small percentage of Type II bipolar cells and ganglion cells.     

GABA-like immunoreactivity in the macaque monkey retina: a light and electron microscopic study

The distribution of GABA-like immunoreactivity in the macaque monkey retina was studied by using postembedding techniques on semithin and ultrathin sections. At the light microscopic level, both inner and outer plexiform layers showed strong GABA-like immunoreactivity in the central retina. All the horizontal cells, some bipolar cells, 30-40% of amacrine cells, occasional interplexiform cells, and practically all displaced amacrine cells were labeled. In the peripheral retina (beyond 5 mm eccentricity), the outer plexiform layer and the horizontal cells were not labeled, but all other cell types showed the same labeling pattern as in the central retina. Synapses of the inner plexiform layer involving a pre- or postsynaptic GABA-labeled process were studied electron microscopically. Synapses involving a GABA-labeled presynaptic amacrine cell process made up 80% of the synapses observed. These GABA-labeled amacrine processes synapsed onto amacrine, bipolar, and ganglion cell processes as well as onto amacrine and ganglion cell bodies. Synapses involving a postsynaptic GABA-labeled process made up 20% of the synapses studied. The GABA-like immunoreactive processes were postsynaptic to bipolar cells at the dyads and to amacrine cells at conventional synapses.     

Somatostatin-like immunoreactive material in the rabbit retina: immunohistochemical staining using monoclonal antibodies

Two mouse monoclonal antibodies to somatostatin-14 were used with avidin-biotin-peroxidase immunohistochemical technique to examine the rabbit retina. In agreement with a previous study using a polyclonal anti-serum, a sparse population (about 1,000 per retina) of neurons in the ganglion cell layer are immunoreactive for somatostatin; the vast majority of these cells are inferior to the myelinated fiber bundle. In addition, the monoclonal antibodies disclose a second neuronal population that forms a circumferential band of immunoreactive neurons around the extreme periphery of the retina. The cells in the body of the inferior retina have dendrites that ramify in the inner plexiform layer. Both the circumferential band of cells and the cells in the body of the inferior retina give off axonlike processes that run in the inner plexiform layer and do not enter the optic nerve. These long, straight varicose fibers form a meshwork that covers the entire retina. The superior retina, which contains only rare immunoreactive cell bodies, has a plexus of stained fibers comparable to that of the inferior retina. The circumferential band of cells is relatively resistant to the neurotoxin kainic acid, explaining a previously reported observation that this toxin depletes only about 50% of the content of somatostatin-like immunoreactivity from the rabbit retina. Moreover, the somatostatin immunoreactive neurons are not labeled by the intraocular injection of the fluorescent dye DAPI, which labels the cholinergic displaced amacrine cells of the rabbit retina. These observations imply that somatostatin-like immunoreactivity is localized to two populations of associational ganglion cells, neurons with cell bodies in the ganglion cell layer, the axons of which remain within the retina.     

Electron microscopical observations on the indoleamine-accumulating neurons and their synaptic connections in the retina of the cat

The distribution of indoleamine-accumulating amacrine cells and their synaptic connections in the retina of the cat were analyzed in the fluorescence, phase-contrast, and electron microscopes. The findings were compared to recently characterized morphological subclasses of amacrine cells. The indoleamine-accumulating neurons were visualized after labeling with an exogenous indoleamine, 5, 6-dihydroxytryptamine. The intravitreal injection of the labeling drug was preceded by treatment with the neurotoxic dopamine-analogue, 6-hydroxydopamine, in order to destroy the otherwise interfering dopaminergic processes. The analysis in the fluorescence and phase-contrast microscopes confirmed earlier reports that the indoleamine-accumulating cell bodies and processes have a distribution consistent with that of amacrine cells. A stratified branching pattern of the indoleamine-accumulating processes in the outer half of the inner plexiform layer was discovered. In the inner half of that layer the branching pattern is diffuse. In the electron microscope the indoleamine-accumulating neurons were seen to have synapses of the conventional type. Their main synaptic contacts are reciprocal synapses with rod bipolar terminals in sublamina b of the inner plexiform layer. They also have synapses with flat cone bipolar terminals in sublamina a, and occasionally with amacrine cells and ganglion cells throughout the inner plexiform layer. Synapses with invaginating cone bipolar terminals, in sublamina b, appear to be rare. The synaptic arrangement with reciprocal synapses with rod bipolar terminals is similar to that of the recently reported AI amacrine cells. It is also similar to that of the indoleamine-accumulating neurons in the retinae of other mammals investigated earlier.     

Horizontal cells of the mouse retina contain glutamic acid decarboxylase-like immunoreactivity during early developmental stages

We have used an antiserum to L-glutamic acid decarboxylase ((GAD), a synthesizing enzyme for gamma-aminobutyric acid (GABA)) to localize putative GABAergic neurons in the developing C57BL/6J mouse retina. At early developmental stages (embryonic day 17 to postnatal day 3), strong GAD-like immunoreactivity is detectable in cell bodies located within the neuroblastic layer. These cells have relatively large cell bodies and extend several sturdy processes which are oriented radially at these early stages. We have identified these cells as horizontal cells. In addition, cell bodies adjacent to the inner plexiform layer and both diffuse and punctate structures within the inner plexiform layer proper have weak GAD-like immunoreactivity at this time. By postnatal day 6, GAD-positive horizontal cell processes begin to form a horizontal network in the newly formed outer plexiform layer. Immunolabeling of amacrine cell bodies and of punctate structures in the inner plexiform layer becomes much stronger at this time, reaching a maximum staining intensity during the second postnatal week. After postnatal day 12, GAD-like immunoreactivity of the horizontal cells begins to decline; in 4-week-old mice the horizontal cells are no longer detectably labeled by this GAD antiserum. At the same time, the GAD-like-immunoreactive material in the inner plexiform layer becomes stratified, forming distinct layers. Amacrine cells and the inner plexiform layer remain GAD positive into adulthood.     

Glutamate receptor agonists release [3H]GABA preferentially from horizontal cells

A total of 5-6 different cell types in vertebrate retinas accumulate [3H]gamma-aminobutyric acid (GABA). In frog retina, specific populations of cells in the horizontal, amacrine and ganglion cell layers are labeled autoradiographically after a 15-min in vitro incubation with [3H]GABA. Cells which may be bipolar or interplexiform cells are also labeled. Similar autoradiographic patterns are observed in chick retina except for the absence of labeled bipolar or interplexiform cells. In rat retinas, [3H]GABA uptake is limited primarily to Muller and amacrine cells. Depolarizing glutamate receptor agonists (glutamate, aspartate and kainic acid) applied in an in vitro perfusion system, stimulated massive release of [3H]GABA from frog and chick retina but not from rat retina. Under these conditions, autoradiographic labeling of horizontal cells was virtually depleted, while labeling of other cell types remained robust. In contrast, potassium caused release of the label from all 3 types of retina, and loss of autoradiographic labeling occurred uniformly in all cell types. We conclude that [3H]GABA-accumulating horizontal cells possess depolarizing glutamate receptors and that activation of these receptors leads to a release of GABA stores. On the other hand, Muller cells and the various subclasses of [3H]GABA-accumulating amacrine, bipolar and/or interplexiform cells, do not release GABA in response to glutamate receptor stimulation and thus appear to be relatively insensitive to excitatory amino acids.     

Localization of L-glutamic acid decarboxylase mRNA in cat retinal horizontal cells by in situ hybridization

Retinal horizontal cells receive synaptic input from photoreceptors and provide a pathway for lateral interactions in the vertebrate retina. In nonmammalian retinas, the H1 horizontal cells appear to use gamma-amino butyric acid (GABA) as their neurotransmitter. The transmitter used by mammalian horizontal cells, however, remains to be identified. In the present study, we have employed in situ hybridization to examine whether cat retinal horizontal cells contain L-glutamic acid decarboxylase (GAD) mRNA and hence might use GABA as their transmitter. In the cat retina, labeled cell bodies were found in the inner nuclear layer and the ganglion cell layer. No labeled cells were found in the photoreceptor layer. In the inner nuclear layer, labeled somata were present at two locations. The majority of them (approximately 72%) were located in the vitread side of the inner nuclear layer bordering the inner nuclear layer/inner plexiform layer boundary. A second class of labeled cells in the inner nuclear layer (approximately 20%) had larger somata and were present at the inner nuclear layer/outer plexiform layer boundary. Double labeling experiments with antisera to parvalbumin, a horizontal cell marker, showed that these perikarya belonged to horizontal cells. RNA blot analysis showed that cat retina contains a single species of GAD mRNA that is about 4 kb in size. These data show that in addition to GABAergic amacrine, displaced amacrine, and interplexiform cells described previously, horizontal cells contain GAD mRNA and may use GABA as their neurotransmitter. Hence, GABA may be a transmitter that is involved in lateral inhibition in both nonmammalian and mammalian retinas.     

Localization of putative GABAergic neurons in the larval tiger salamander retina by immunocytochemical and autoradiographic methods

Putative GABAergic neurons in the larval tiger salamander retina were localized by a comparative analysis of glutamate decarboxylase immunoreactivity (GAD-IR), GABA-like immunoreactivity (GABA-IR), and high-affinity 3H-GABA uptake at the light microscopical level. Preliminary data showed that all GAD-IR neurons were double labeled for GABA-IR. However, because the weak somatic labeling with GAD-IR, we could not determine if the converse were true. Neurons commonly labeled with GABA-IR and 3H-GABA uptake include horizontal cells, type I (outer) and type II (inner) bipolar cells, type I (inner) and type II (outer) amacrine cells, and cell bodies in the ganglion cell layer (GCL). In addition, interplexiform cells were identified with GABA-IR. The presence of GABA-IR ganglion cells was indicated by GABA-IR fibers in the optic fiber layer and optic nerve as well as by a GABA-IR cell in the GCL that included a labeled axon. The percentage of labeled somas in the inner nuclear layer (INL) compared to all cells in each layer was similar for the two methods: 30% in INL 1 (outer layer of somas), 15% in INL 2 (middle layer), 43-52% in INL 3 (inner layer), and about 21-26% in the GCL. Labeled processes were found in three bands in the inner plexiform layer, with the densest band located in the most proximal part. Postembedding labeling of 1-micron Durcupan resin sections for GABA-IR showed the same general pattern as obtained with 10-microns cryostat sections, with additional staining, however, of type II (inner) bipolar cell Landolt's clubs. Extensive colocalization of labeling was indicated, and we conclude that GABA-IR can serve as a valid and reliable marker for GABA-containing neurons in this retina and suggest that GABA serves as a transmitter for horizontal cells, several types of amacrine cell, a type of interplexiform cell, and perhaps a small percentage of type I and type II bipolar cells and ganglion cells.     

Localization of kainic acid-sensitive cells in mammalian retina

Short-term (15 minutes) in vitro exposure to kainic acid (KA), a rigid structural analog of L-glutamic acid (Glu), caused two morphologically distinct neuronal lesions in retinas of several species. In rabbit retina, one type of lesion was characterized by rapid swelling after exposure to low concentrations of KA (10^?4 M). This lesion was observed in elements of both plexiform layers and, more specifically, in cell bodies and neurites of horizontal cells that contact cones. A few cell bodies from the amacrine cell layer showed some limited swelling. The swelling was completely blocked when sodium was removed from the incubation medium. The second type of lesion was generally seen after longer exposures of after exposure to higher concentrations of KA and was evidenced by degeneration of neurons in the amacrine and ganglion cell layers. One exception was noted in that a few cells from the ganglion cell layer degenerated even under low exposure conditions. The second type of lesion was not blocked by removal of sodium ions. Photoreceptor cells appeared resistant to all effects of KA. The results suggest that a correlation may exist between certain KA-induced lesions of the retina and putative glutamoreceptive neurons. At the same time, the two types of retinal lesions produced by KA are morphologically and chemically differentiable and may be useful in elucidating the differences between specific, Glu-related toxicity and nonspecific toxicity of KA.     

Localization of GABAA receptor subunits alpha 1, alpha 3, beta 1, beta 2/3, gamma 1, and gamma 2 in the salamander retina

Electrophysiological studies have demonstrated that gamma-aminobutyric acid receptors type A (GABA(A)) mediate important information processing in the retinas of salamander and other vertebrates. The pharmacology and physiology of GABA(A) receptors depend on their subunit composition. We studied the localization of GABA(A) receptor subunit isoforms alpha(1), alpha(3), beta(1), beta(2/3) (antibody BD-17 and 62-3G1), gamma(1), and gamma(2) in salamander retina with immunocytochemical methods. All three beta-subunit antibodies labeled similarly in the outer retina, especially the inner segments and synaptic terminals of rod photoreceptors (identified with protein kinase C). Somatic labeling was observed in cell bodies of some horizontal cells, bipolar cells, amacrine cells, and cells in the ganglion cell layer (GCL). Puncta were present throughout the inner plexiform layer (IPL) for beta(1) and 62-3G1, but not for BD-17. alpha(1)-immunoreactivity (IR) stained a population of presumed OFF rod-dominated bipolar cells, including dendrites, soma, and axon terminals in the distal IPL. A subtype of GABAergic amacrine cell also expressed alpha(1)-IR, with puncta sparsely distributed at the distal and proximal margins of the IPL. Both the OPL and IPL were labeled throughout for alpha(3)-IR, as opposed to the narrow distribution of alpha(1)-IR in the IPL, suggesting that the two alpha-subunits are localized at different synaptic sites. Punctate gamma(1)-IR was observed in the OPL and IPL, whereas gamma(2) was most prominent in cone photoreceptors (identified with calbindin), including the terminal telodendria, in cell bodies of some horizontal cells, amacrine cells, cells in the GCL, and less intensely in the IPL. In addition, several subunits were present in Müller cells. The differential labeling suggests the existence of GABA(A) receptor subtypes with different subunit compositions that mediate multiple GABAergic functions in salamander retina.     

Localization of aspartate-like immunoreactivity in the retina of the turtle (Pseudemys scripta).

Aspartate has been reported to be a putative excitatory neurotransmitter in the retina, but little detailed information is available concerning its anatomical distribution. We used an antiserum directed against an aspartate-albumin conjugate to analyze the anatomy, dendritic stratification, and regional distribution of cell types with aspartate-like immunoreactivity in the turtle retina. The results showed dramatic differences in immunoreactivity in the peripheral versus the central retina. Strong aspartate-like immunoreactivity was shown in the peripheral retina, with many well-labeled processes in the inner plexiform layer. Many bipolar, horizontal, amacrine, and ganglion cells, some photoreceptors, and some unidentified cells were strongly immunoreactive in the peripheral retina. In contrast, although the central retina showed well-labeled horizontal cells, there was only light labeling in the inner plexiform layer with weakly immunoreactive amacrine and ganglion cells and no labeled bipolar cells. There were several strongly immunoreactive efferent nerve fibers which left the optic nerve head and arborized extensively in the retina. At the electron microscopic level, electron-dense reaction product was associated with synaptic vesicles at bipolar and amacrine cell synapses in the inner plexiform layer. These results suggest that aspartate may be involved in many diverse synaptic interactions in both the outer plexiform layer and the inner plexiform layer of the turtle retina.     

(3H) glycine-accumulating neurons of the human retina

Isolated human retinas were incubated in physiological saline containing micromolar (3H) glycine. The types, distributions, and synaptologies of glycine-accumulating neurons were determined by light and electron microscope autoradiography. Two types of amacrine cells were discriminated on the bases of number of processes descending into the inner plexiform layer, density of label in light-microscope autoradiographs, size, and synaptic features: (1) Gly1 amacrine cells have moderate labeling, several oblique dendrites arising from the soma, and electron lucent synaptic terminals containing large presynaptic specializations, nd (2) Gly2 amacrine cells have dense labeling, a single proximal dendrite, and moderately electron-dense terminals with small presynaptic specializations. Gly1 amacrine cells constitute approximately 15% and Gly2 amacrine cells approximately 38% of all cells in the amacrine cell layer. The laminar distribution of label in the inner plexiform layer was measured by scanning microdensitometry, which provided a format for categorizing types of synaptic contacts. Many features of glycine-accumulating amacrine cell contacts were similar to those of cat AII/Gly2 amacrine cells: a diffuse yet bisublaminar distribution of label, concentration of synaptic output in sublamina a, rod bipolar cell input in sublamina b and gap junctions in mid-inner plexiform layer involving labeled cells. The evidence seems to indicate that human Gly2 amacrine cells and cat AII/Gly2 amacrine cells are homologous cell types. finally, some cone bipolar cells were labeled.     

Identification and characterization of an aquaporin 1 immunoreactive amacrine-type cell of the mouse retina

Using immunocytochemistry, a type of amacrine cell that is immunoreactive for aquaporin 1 was identified in the mouse retina. AQP1 immunoreactivity was found in photoreceptor cells of the outer nuclear layer (ONL) and in a distinct type of amacrine cells of the inner nuclear layer (INL). AQP1-immunoreactive (IR) amacrine cell somata were located in the INL and their processes extended through strata 3 and 4 of the inner plexiform layer (IPL) with thin varicosities. The density of the AQP1-IR amacrine cells increased from 100/mm(2) in the peripheral retina to 350/mm(2) in the central retina. The AQP1-IR amacrine cells comprise 0.5% of the total amacrine cells. The AQP1-IR amacrine cell bodies formed a regular mosaic, which suggested that they represent a single type of amacrine cell. Double labeling with AQP1 and glycine, gamma-aminobutyric acid (GABA) or GAD(65) antiserum demonstrated that the AQP1-IR amacrine cells expressed GABA or GAD(65) but not glycine. Their synaptic input was primarily from other amacrine cell processes. They also received synaptic inputs from a few cone bipolar cells. The primary synaptic targets were ganglion cells, followed by other amacrine cells and cone bipolar cells. In addition, gap junctions between an AQP1-IR amacrine process and another amacrine process were rarely observed. In summary, a GABAergic amacrine cell type labeled by an antibody against AQP1 was identified in the mouse retina and was found to play a possible role in transferring a certain type of visual information from other amacrine or a few cone bipolar cells primarily to ganglion cells.     

Neuronal subpopulations in cat retina which accumulate the GABA agonist, (3H)muscimol: a combined Golgi and autoradiographic study

Golgi impregnation techniques were combined with electron microscopic autoradiography of (3H-muscimol in order to provide morphological identification of labeled neurons in the cat retina. This gamma-aminobutyric acid (GABA) agonist has been shown to label the same neurons which accumulate (3H)GABA. Selected cells were photographed and drawn by the aid of a camera lucida drawing tube prior to being thin sectioned for autoradiography. The (3H)muscimol-accumulating neurons which were identified include an interplexiform cell, five classes of conventional amacrine cell, and another cell with its soma located in the ganglion cell layer which is either a ganglion cell or a displaced amacrine. The conventional amacrine cells were compared with the recent morphological classification of Kolb et al. (Vision Res. 21: 1081-1114, '81) and identified as A2, A10, A13, A17, and A19 amacrine cells. These cells exhibit a widespread distribution providing input to all five strata of the inner plexiform layer.     

‘Starburst’ amacrine cells and cholinergic neurons: mirror-symmetric ON and OFF amacrine cells of rabbit retina

Golgi-impregnated 'starburst' amacrine cells share significant morphological features with cholinergic neurons in rabbit retina. They are mirror-symmetrical about the a/b (OFF/ON) sublaminar border of the inner plexiform layer. Type a starburst amacrines have cell bodies in the amacrine cell layer and dendrites in sublamina a, while type b cells have their cell bodies in the ganglion cell layer and dendrites in sublamina b of the inner plexiform layer (IPL). The two levels of narrow dendritic stratification are precisely those demonstrated by Masland and Mills for cholinergic amacrine cells. The morphological evidence indicates that the duality of ON and OFF pathways is served separately by type b (displaced) and type a starburst amacrine cells, respectively.