Localization of GABAA receptor subtypes in the tiger salamander retina

1992 ◽  
Vol 8 (1) ◽  
pp. 57-64 ◽  
Author(s):  
Chen-YU Yang ◽  
Zhen-Shi Lin ◽  
Stephen Yazulla
Keyword(s):  
Binding Sites ◽  
Benzodiazepine Receptors ◽  
Plexiform Layer ◽  
Receptor Subtypes ◽  
Tiger Salamander ◽  
Inner Plexiform Layer ◽  
Inner Retina ◽  
Site Specific ◽  
Gabaa Receptor Subtypes ◽  
Muscimol Binding

AbstractDry autoradiography was used to determine the distribution of GABAA binding sites in tiger salamander retina. High-affinity binding of [3H]-flunitrazepam ([3H]-FNZ) was used to localize benzodiazepine receptors (BZR) and [3H]-muscimol was used to localize the GABAA recognition site. Specific [3H]-FNZ binding was present only in the inner retina, primarily in the inner plexiform layer (IPL). Co-incubation with GABA enhanced [3H]-FNZ binding by 20–50%. [3H]-muscimol binding was found throughout the IPL and in the outer plexiform layer (OPL). Mouse monoclonal antibodies 62–3G1 and BD-17, that recognize the GABAAβ2, β3 polypeptides, and BD-24, that recognizes the GABAA α1, polypeptide, did not label either the OPL or IPL, despite numerous variations in the fixation and immunoprocessing methods. GABAA receptor location, as revealed by [3H]-muscimol binding, matches the distribution of presumed GABAergic terminals in the OPL and IPL. We suggest that there are at least two subtypes of GABAA receptor in the tiger salamander retina: one type is present only in the inner retina, primarily in the IPL and is functionally coupled to BZRs; the other type is located in the OPL and is not coupled to the BZRs. Furthermore, GABAA receptors in the tiger salamander retina appear to be of a different epitope than GABAA receptors in numerous other preparations that are recognized by mAbs 62–3G1, BD-17, and BD-24.

scholarly journals Morphology of Inner Retina in Rhesus Monkeys of Various Ages: A Comparative Study

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Jingfei Chen ◽  
Qihui Luo ◽  
Chao Huang ◽  
Wen Zeng ◽  
Ping Chen ◽  
...  
Keyword(s):  
Rhesus Monkeys ◽  
Morphological Structure ◽  
Plexiform Layer ◽  
Bipolar Cells ◽  
Growth Stages ◽  
Retinal Layer ◽  
Inner Plexiform Layer ◽  
Fiber Layer ◽  
Inner Retina ◽  
Biological Studies

Purpose. To investigate the changes of thickness in each layer, the morphology and density of inner neurons in rhesus monkeys’ retina at various growth stages, thus contribute useful data for further biological studies. Methods. The thickness of nerve fiber layer (NFL), the whole retina, inner plexiform layer (IPL), and outer plexiform layer (OPL) of rhesus monkeys at different ages were observed with hematoxylin and eosin (H&E) staining. The morphology and the density of inner neurons of rhesus monkey retina were detected by immunofluorescence. Results. The retina showed the well-known ten layers, the thickness of each retinal layer in rhesus monkeys at various ages increased rapidly after infant, and the retina was the thickest in adulthood, but the retinal thickness stop growing in senescent. Quantitative analysis showed that the maximum density of inner neurons was reached in adolescent, and then, the density of inner neurons decreased in adults and senescent retinas. And some changes in the morphology of rod bipolar cells have occurred in senescent. Conclusions. The structure of retina in rhesus monkeys is relatively immature at infant, and the inner retina of rhesus monkeys is mature in adolescent, while the thickness of each retinal layer was the most developed in the adult group. There was no significant change in senescence for the thickness of each retinal layer, but the number of the neurons in our study has a decreasing trend and the morphological structure has changed.

Regional distribution of nitrergic neurons in the inner retina of the chicken

2011 ◽  
Vol 28 (3) ◽  
pp. 205-220 ◽  
Author(s):  
MARTIN WILSON ◽  
NICK NACSA ◽  
NATHAN S. HART ◽  
CYNTHIA WELLER ◽  
DAVID I. VANEY
Keyword(s):  
Ganglion Cell ◽  
Ganglion Cells ◽  
Regional Distribution ◽  
Plexiform Layer ◽  
Visual Image ◽  
Amacrine Cells ◽  
Cell Types ◽  
Inner Plexiform Layer ◽  
Inner Retina ◽  
Neuronal Types

AbstractUsing both NADPH diaphorase and anti-nNOS antibodies, we have identified—from retinal flatmounts—neuronal types in the inner retina of the chicken that are likely to be nitrergic. The two methods gave similar results and yielded a total of 15 types of neurons, comprising 9 amacrine cells, 5 ganglion cells, and 1 centrifugal midbrain neuron. Six of these 15 cell types are ubiquitously distributed, comprising 3 amacrine cells, 2 displaced ganglion cells, and a presumed orthotopic ganglion cell. The remaining nine cell types are regionally restricted within the retina. As previously reported, efferent fibers of midbrain neurons and their postsynaptic partners, the unusual axon-bearing target amacrine cells, are entirely confined to the ventral retina. Also confined to the ventral retina, though with somewhat different distributions, are the “bullwhip” amacrine cells thought to be involved in eye growth, an orthotopic ganglion cell, and two types of large axon-bearing amacrine cells whose dendrites and axons lie in stratum 1 of the inner plexiform layer (IPL). Intracellular fills of these two cell types showed that only a minority of otherwise morphologically indistinguishable neurons are nitrergic. Two amacrine cells that branch throughout the IPL are confined to an equatorial band, and one small-field orthotopic ganglion cell that branches in the proximal IPL is entirely dorsal. These findings suggest that the retina uses different processing on different regions of the visual image, though the benefit of this is presently obscure.

Modulation of the components of the rat dark-adapted electroretinogram by the three subtypes of GABA receptors

2003 ◽  
Vol 20 (5) ◽  
pp. 535-542 ◽  
Author(s):  
ANNA MÖLLER ◽  
THOR EYSTEINSSON
Keyword(s):  
Gaba Receptors ◽  
Plexiform Layer ◽  
Amacrine Cells ◽  
Electric Activity ◽  
Oscillatory Potentials ◽  
Receptor Subtypes ◽  
Inner Plexiform Layer ◽  
Receptor Ligands ◽  
Cellular Origin ◽  
Stimulation Of

The separate components of the dark-adapted electroretinogram (ERG) are believed to reflect the electric activity of neurones in both the inner and the outer layers of the retina, although their precise origin still remains unclear. The purpose of this study was to examine whether selective blockage or stimulation of the different subtypes of GABA receptors might help further elucidate the cellular origin of the components of the dark-adapted ERG. The rat retina is of interest since the localization and physiology of GABA receptors in that retina have been examined in great detail. GABA agonists and antagonists, known to affect the responses of neurons in the inner plexiform layer, were injected into the vitreous of one eye while ERG responses evoked by flashes of white light were recorded. GABA and the GABAa agonist isoguvacine completely removed the oscillatory potentials (OPs) and reduced the amplitude of the a- and b-waves. TPMPA, a GABAc antagonist, reduced the a- and b-waves but had no significant effect on the OPs. Baclofen, a GABAb agonist, reduced the amplitude of the a- and b-waves, without having any effects on the amplitude of the OPs. The GABAb antagonist CGP35348 increased the amplitudes of the a- and b-wave without having an effect on the amplitudes of the OPs. The GABAb receptor ligands had significant and opposite effect on the latency of the OPs. These results indicate that retinal neurons, presumably a subpopulation of amacrine cells, that have GABAb receptors are not the source of the OPs of the ERG, although they may modulate these wavelets in some manner, while contributing to the generation of the dark-adapted a- and b-waves. OPs are modified by stimulation of GABAa receptors, and the a- and b-waves by stimulation of all GABA receptor subtypes.

M-wave of the toad electroretinogram

1991 ◽  
Vol 66 (6) ◽  
pp. 1927-1940 ◽  
Author(s):  
B. J. Katz ◽  
R. Wen ◽  
J. B. Zheng ◽  
Z. A. Xu ◽  
B. Oakley
Keyword(s):  
Plexiform Layer ◽  
Müller Cell ◽  
Inner Plexiform Layer ◽  
Excitatory Effect ◽  
Inner Retina ◽  
M Wave ◽  
Threshold Response ◽  
Slow Piii ◽  
Muller Cell ◽  
Toad Bufo

1. In the retina, two distinct, light-evoked releases of K+ have been described. One takes place in the outer plexiform layer (OPL) and is termed the "distal K+ increase." The other takes place in the inner plexiform layer (IPL) and is termed the "proximal K+ increase." Although the distal K+ increase generates the electroretinogram (ERG) b-wave, the contribution of the much larger proximal K+ increase to the ERG is less well understood. In this paper we detail our investigation of the proximal K+ increase and its contribution to the ERG. We describe an ERG component, the M-wave, which had not heretofore been observed in the diffuse-flash, vitreal ERG. 2. We studied the proximal K+ increase and the ERG M-wave in the isolated retina preparation of the toad, Bufo marinus. We used K(+)-sensitive microelectrodes, as well as conventional intra- and extracellular microelectrodes, to record K+ changes, the local (or intraretinal) ERG, the vitreal ERG, and Muller cell responses. 3. As in earlier studies of the amphibian and cat M-wave, we readily observed an M-wave in the intraretinal, or local, ERG (LERG). The M-wave we studied had characteristics similar to those of M-waves that were previously described. Specifically, we found that the M-wave was generated by a Muller cell response to the proximal K+ increase and that both the proximal K+ increase and the LERG M-wave were spatially tuned. 4. We used the aspartate receptor agonist, N-methyl-DL-aspartate (NMA), to reveal that an M-wave is present in the vitreal ERG. Researchers who previously investigated the M-wave were unable to identify an M-wave in the vitreal ERG. We found that the toad ERG M-wave was a small, positive potential that was partially obscured by the much larger b-wave and slow PIII components. 5. We observed that picrotoxin (PTX) had an excitatory effect on inner retina, as evidenced by an enhanced proximal K+ increase and an enhanced M-wave. This result indicates that it is likely that GABAergic inhibition in inner retina plays an important role in retinal processing in the toad. 6. At threshold, we found that the ERG consisted mainly of an M-wave, indicating that the amphibian threshold ERG is driven by proximal retina. This result is analogous to previous observations of the threshold ERG in cat. However, in cat, the M-wave and threshold response have been described as distinct ERG components.(ABSTRACT TRUNCATED AT 400 WORDS)

Immunocytochemical localization of excitatory and inhibitory neurotransmitters in the zebrafish retina

1999 ◽  
Vol 16 (3) ◽  
pp. 483-490 ◽  
Author(s):  
V.P. CONNAUGHTON ◽  
T.N. BEHAR ◽  
W.-L.S. LIU ◽  
S.C. MASSEY
Keyword(s):  
Ganglion Cells ◽  
Plexiform Layer ◽  
Amacrine Cells ◽  
Bipolar Cells ◽  
Acid Decarboxylase ◽  
Inner Plexiform Layer ◽  
Immunocytochemical Localization ◽  
Inner Retina ◽  
Light Microscope Level ◽  
Axon Terminals

The patterns of glutamate, γ-aminobutyric acid (GABA), and glycine distribution in the zebrafish retina were determined using immunocytochemical localization of antisera at the light-microscope level. The observed GABA immunoreactivity (GABA-IR) patterns were further characterized using antibodies to both isoforms of glutamic acid decarboxylase (GAD65 and GAD67), the synthetic enzyme for GABA. Glutamate-IR was observed in all retinal layers with photoreceptors, bipolar cells, and ganglion cells prominently labeled. Bipolar cells displayed the most intense glutamate-IR and bipolar cell axon terminals were clearly identified as puncta arranged in layers throughout the inner plexiform layer (IPL). These findings suggest the presence of multiple subtypes of presumed OFF- and ON-bipolar cells, including some ON-bipolar cells characterized by a single, large (9 μm × 6 μm) axon terminal. GABA-, GAD-, and glycine-IR were most intense in the inner retina. In general, the observed labeling patterns for GABA, GAD65, and GAD67 were similar. GABA- and GAD-IR were observed in a population of amacrine cells, a few cells in the ganglion cell layer, throughout the IPL, and in horizontal cells. In the IPL, both GABA- and GAD-IR structures were organized into two broad bands. Glycine-IR was observed in amacrine cells, interplexiform cells, and in both plexiform layers. Glycine-positive terminals were identified throughout the IPL, with a prominent band in sublamina 3 corresponding to an immunonegative region observed in sections stained for GAD and GABA. Our results show the distribution of neurons in the zebrafish retina that use glutamate, GABA, or glycine as their neurotransmitter. The observed distribution of neurotransmitters in the inner retina is consistent with previous studies of other vertebrates and suggests that the advantages of zebrafish for developmental studies may be exploited for retinal studies.

Modulation of Excitatory Synaptic Transmission by GABAC Receptor-Mediated Feedback in the Mouse Inner Retina

2001 ◽  
Vol 86 (5) ◽  
pp. 2285-2298 ◽  
Author(s):  
Ko Matsui ◽  
Jun Hasegawa ◽  
Masao Tachibana
Keyword(s):  
Nmda Receptors ◽  
Time Course ◽  
Feedback Inhibition ◽  
Plexiform Layer ◽  
Amacrine Cells ◽  
Bipolar Cells ◽  
Mouse Retina ◽  
Receptor Subtypes ◽  
Inner Plexiform Layer ◽  
Cone Bipolar Cells

In many vertebrate CNS synapses, the neurotransmitter glutamate activates postsynaptic non- N-methyl-d-aspartate (NMDA) and NMDA receptors. Since their biophysical properties are quite different, the time course of excitatory postsynaptic currents (EPSCs) depends largely on the relative contribution of their activation. To investigate whether the activation of the two receptor subtypes is affected by the synaptic interaction in the inner plexiform layer (IPL) of the mouse retina, we analyzed the properties of the light-evoked responses ofon-cone bipolar cells and on-transient amacrine cells in a retinal slice preparation. on-transient amacrine cells were whole cell voltage-clamped, and the glutamatergic synaptic input from bipolar cells was isolated by a cocktail of pharmacological agents (bicuculline, strychnine, curare, and atropine). Direct puff application of NMDA revealed the presence of functional NMDA receptors. However, the light-evoked EPSC was not significantly affected byd(−)-2-amino-5-phosphonopentanoic acid (d-AP5), but suppressed by 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX) or 1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine hydrochloride (GYKI 52466). These results indicate that the light-evoked EPSC is mediated mainly by AMPA receptors under this condition. Since bipolar cells have GABACreceptors at their terminals, it has been suggested that bipolar cells receive feedback inhibition from amacrine cells. Application of (1,2,5,6-tetrahydropyridin-4-yl)methylphosphinic acid (TPMPA), a specific blocker of GABAC receptors, suppressed both the GABA-induced current and the light-evoked feedback inhibition observed in on-cone bipolar cells and enhanced the light-evoked EPSC of on-transient amacrine cells. In the presence of TPMPA, the light-evoked EPSC of amacrine cells was composed of AMPA and NMDA receptor-mediated components. Our results suggest that photoresponses of on-transient amacrine cells in the mouse retina are modified by the activation of presynaptic GABAC receptors, which may control the extent of glutamate spillover.

Roles of aspartate and glutamate in synaptic transmission in rabbit retina. II. Inner plexiform layer

1985 ◽  
Vol 53 (3) ◽  
pp. 714-725 ◽  
Author(s):  
S. A. Bloomfield ◽  
J. E. Dowling
Keyword(s):  
Membrane Potential ◽  
Bipolar Cell ◽  
Ganglion Cells ◽  
Plexiform Layer ◽  
Bipolar Cells ◽  
Inner Plexiform Layer ◽  
Retinal Neurons ◽  
Inner Retina ◽  
Axon Terminals ◽  
Cell Responses

Intracellular recordings were obtained from amacrine and ganglion cells in the superfused, isolated retina-eyecup of the rabbit. The putative neurotransmitters aspartate, glutamate, and several of their analogues were added to the superfusate while the membrane potential and light-responsiveness of the retinal neurons were monitored. Both L-aspartate and L-glutamate displayed excitatory actions on the activity of the vast majority of amacrine and ganglion cells studied. However, these agents occasionally appeared to inhibit the responses of the inner retinal neurons by producing hyperpolarization of the membrane potential and blockage of the light-evoked responses. In either case, the effects of aspartate and glutamate were indistinguishable. The glutamate analogues kainate and quisqualate produced strong excitatory effects on the responses of amacrine and ganglion cells at concentrations some 200-fold less than those needed to obtain similar effects with aspartate or glutamate. The aspartate analogue, n-methyl DL-aspartate (NMDLA), also produced strong excitatory effects but was approximately three times less potent than kainate or quisqualate. On one occasion, we encountered a ganglion cell that was depolarized by kainate, but hyperpolarized by NMDLA. The glutamate antagonist alpha-methyl glutamate and the aspartate antagonist alpha-amino adipate effectively blocked the responses of amacrine and ganglion cells. However, on any one cell, one antagonist was always clearly more potent than the other. We examined the actions of the glutamate analogue 2-amino-4-phosphonobutyrate (APB) on the responses of inner retinal neurons and found that it selectively abolished all "on" activity in the inner retina. Together with our finding that APB selectively abolishes on-bipolar cell responses (see Ref. 6), these data support the hypothesis that on-bipolar cells subserve the "on" activity of amacrine and ganglion cells. Our data suggest that aspartate and glutamate are excitatory transmitters in the inner retina, possibly being released from bipolar cell axon terminals in the inner plexiform layer.

scholarly journals Spatial and temporal distribution patterns of Na-K-2Cl cotransporter in adult and developing mouse retinas

2008 ◽  
Vol 25 (2) ◽  
pp. 109-123 ◽  
Author(s):  
BAOQIN LI ◽  
KELLI McKERNAN ◽  
WEN SHEN
Keyword(s):  
Temporal Distribution ◽  
Plexiform Layer ◽  
Distribution Patterns ◽  
Bipolar Cells ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Mouse Retina ◽  
Inner Plexiform Layer ◽  
Inner Retina ◽  
Adult Mice

AbstractThe Na-K-2Cl cotransporter (NKCC) is a Cl− uptake transporter that is responsible for maintaining a Cl− equilibrium potential positive to the resting potential in neurons. If NKCC is active, GABA and glycine can depolarize neurons. In view of the abundance of GABAergic and glycinergic synapses in retina, we undertook a series of studies using immunocytochemical techniques to determine the distribution of NKCC in retinas of both developing and adult mice. We found NKCC antibody (T4) labeling present in retinas from wild-type mice, but not in NKCC1-deficient mice, suggesting that the NKCC1 subtype is a major Cl− uptake transporter in mouse retina. Strong labeling of NKCC1 was present in horizontal cells and rod-bipolar dendrites in adult mice. Interestingly, we also found that a diffuse labeling pattern was present in photoreceptor terminals. However, NKCC1 was barely detectable in the inner retina of adult mice. Using an antibody against K-Cl cotransporter 2 (KCC2), we found that KCC2, a transporter that extrudes Cl−, was primarily expressed in the inner retina. The expression of NKCC1 in developing mouse retinas was studied from postnatal day (P) 1 to P21, NKCC1 labeling first appeared in the dendrites of horizontal and rod-bipolar cells as early as P7, followed by photoreceptor terminals between P10-P14; with expression gradually increasing concomitantly with the growth of synaptic terminals and dendrites throughout retinal development. In the inner retina, NKCC1 labeling was initially observed in the inner plexiform layer at P1, but labeling diminished after P5. The developmental increase in NKCC expression only occurred in the outer retina. Our results suggest that the distal synapses and synaptogenesis in mouse retinas undergo a unique process with a high intracellular Cl− presence due to NKCC1 expression.

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