IN MEMORIAM
In memoriam
- ROBERT F. MILLER, ELIO RAVIOLA
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- 28 September 2007, pp. 445-447
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The vision research community lost a valuable colleague and friend when Ramon (Ray) Dacheux II died on May 30, 2006 at his home in Birmingham, Alabama. Ray was 58 and had been ill with a brain tumor for two years.
Research Article
Functional polarity of dendrites and axons of primate A1 amacrine cells
- CHRISTOPHER M. DAVENPORT, PETER B. DETWILER, DENNIS M. DACEY
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- 29 May 2007, pp. 449-457
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The A1 cell is an axon-bearing amacrine cell of the primate retina with a diffusely stratified, moderately branched dendritic tree (∼400 μm diameter). Axons arise from proximal dendrites forming a second concentric, larger arborization (>4 mm diameter) of thin processes with bouton-like swellings along their length. A1 cells are ON-OFF transient cells that fire a brief high frequency burst of action potentials in response to light (Stafford & Dacey, 1997). It has been hypothesized that A1 cells receive local input to their dendrites, with action potentials propagating output via the axons across the retina, serving a global inhibitory function. To explore this hypothesis we recorded intracellularly from A1 cells in an in vitro macaque monkey retina preparation. A1 cells have an antagonistic center-surround receptive field structure for the ON and OFF components of the light response. Blocking the ON pathway with L-AP4 eliminated ON center responses but not OFF center responses or ON or OFF surround responses. Blocking GABAergic inhibition with picrotoxin increased response amplitudes without affecting receptive field structure. TTX abolished action potentials, with little effect on the sub-threshold light response or basic receptive field structure. We also used multi-photon laser scanning microscopy to record light-induced calcium transients in morphologically identified dendrites and axons of A1 cells. TTX completely abolished such calcium transients in the axons but not in the dendrites. Together these results support the current model of A1 function, whereby the dendritic tree receives synaptic input that determines the center-surround receptive field; and action potentials arise in the axons, which propagate away from the dendritic field across the retina.
Response properties of a unique subtype of wide-field amacrine cell in the rabbit retina
- STEWART A. BLOOMFIELD, BÉLA VÖLGYI
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- 29 May 2007, pp. 459-469
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We studied the morphology and physiology of a unique wide-field amacrine cell in the rabbit retina. These cells displayed a stereotypic dendritic morphology consisting of a large, circular and monostratified arbor that often extended over 2 mm. Their responses contained both somatic and dendritic sodium spikes suggesting active propagation of synaptic signals within the dendritic arbor. This idea is supported by the enormous size of their ON-OFF receptive fields. Interestingly, these cells exhibited separate ON and OFF receptive fields that, while concentric, were vastly different in size. Whereas the ON receptive field of these cells extended nearly 2 mm, the OFF receptive field was typically 75% smaller. Blockade of voltage-gated sodium channels with QX-314 dramatically reduced the large ON receptive field, but had little effect on the smaller OFF receptive field. These results indicate a spatial disparity in the location of on- and off-center bipolar cell inputs to the dendritic arbor of wide-field amacrine cells. In addition, the active propagation of signals suggests that synaptic inputs are integrated both locally and globally within the dendritic arbor.
Glycine receptors of A-type ganglion cells of the mouse retina
- SRIPARNA MAJUMDAR, LIANE HEINZE, SILKE HAVERKAMP, ELENA IVANOVA, HEINZ WÄSSLE
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- 29 May 2007, pp. 471-487
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A-type ganglion cells of the mouse retina represent the visual channel that transfers temporal changes of the outside world very fast and with high fidelity. In this study we combined anatomical and physiological methods in order to study the glycinergic, inhibitory input of A-type ganglion cells. Immunocytochemical studies were performed in a transgenic mouse line whose ganglion cells express green fluorescent protein (GFP). The cells were double labeled for GFP and the four α subunits of the glycine receptor (GlyR). It was found that most of the glycinergic input of A-type cells is through fast, α1-expressing synapses. Whole-cell currents were recorded from A-type ganglion cells in retinal whole mounts. The response to exogenous application of glycine and spontaneous inhibitory postsynaptic currents (sIPSCs) were measured. By comparing glycinergic currents recorded in wildtype mice and in mice with specific deletions of GlyRα subunits (Glra1spd-ot, Glra2−/−, Glra3−/−), the subunit composition of GlyRs of A-type ganglion cells could be further defined. Glycinergic sIPSCs of A-type ganglion cells have fast kinetics (decay time constant τ = 3.9 ± 2.5 ms, mean ± SD). Glycinergic sIPSCs recorded in Glra2−/− and Glra3−/− mice did not differ from those of wildtype mice. However, the number of glycinergic sIPSCs was significantly reduced in Glra1spd-ot mice and the remaining sIPSCs had slower kinetics than in wildtype mice. The results show that A-type ganglion cells receive preferentially kinetically fast glycinergic inputs, mediated by GlyRs composed of α1 and β subunits.
Robust syntaxin-4 immunoreactivity in mammalian horizontal cell processes
- ARLENE A. HIRANO, JOHANN HELMUT BRANDSTÄTTER, ALEJANDRO VILA, NICHOLAS C. BRECHA
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- 20 July 2007, pp. 489-502
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Horizontal cells mediate inhibitory feed-forward and feedback communication in the outer retina; however, mechanisms that underlie transmitter release from mammalian horizontal cells are poorly understood. Toward determining whether the molecular machinery for exocytosis is present in horizontal cells, we investigated the localization of syntaxin-4, a SNARE protein involved in targeting vesicles to the plasma membrane, in mouse, rat, and rabbit retinae using immunocytochemistry. We report robust expression of syntaxin-4 in the outer plexiform layer of all three species. Syntaxin-4 occurred in processes and tips of horizontal cells, with regularly spaced, thicker sandwich-like structures along the processes. Double labeling with syntaxin-4 and calbindin antibodies, a horizontal cell marker, demonstrated syntaxin-4 localization to horizontal cell processes; whereas, double labeling with PKC antibodies, a rod bipolar cell (RBC) marker, showed a lack of co-localization, with syntaxin-4 immunolabeling occurring just distal to RBC dendritic tips. Syntaxin-4 immunolabeling occurred within VGLUT-1-immunoreactive photoreceptor terminals and underneath synaptic ribbons, labeled by CtBP2/RIBEYE antibodies, consistent with localization in invaginating horizontal cell tips at photoreceptor triad synapses. Vertical sections of retina immunostained for syntaxin-4 and peanut agglutinin (PNA) established that the prominent patches of syntaxin-4 immunoreactivity were adjacent to the base of cone pedicles. Horizontal sections through the OPL indicate a one-to-one co-localization of syntaxin-4 densities at likely all cone pedicles, with syntaxin-4 immunoreactivity interdigitating with PNA labeling. Pre-embedding immuno-electron microscopy confirmed the subcellular localization of syntaxin-4 labeling to lateral elements at both rod and cone triad synapses. Finally, co-localization with SNAP-25, a possible binding partner of syntaxin-4, indicated co-expression of these SNARE proteins in the same subcellular compartment of the horizontal cell. Taken together, the strong expression of these two SNARE proteins in the processes and endings of horizontal cells at rod and cone terminals suggests that horizontal cell axons and dendrites are likely sites of exocytotic activity.
Strychnine, but not PMBA, inhibits neuronal nicotinic acetylcholine receptors expressed by rabbit retinal ganglion cells
- J.M. RENNA, C.E. STRANG, F.R. AMTHOR, K.T. KEYSER
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- 28 September 2007, pp. 503-511
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Strychnine is considered a selective competitive antagonist of glycine gated Cl− channels (Saitoh et al., 1994) and studies have used strychnine at low micromolar concentrations to study the role of glycine in rabbit retina (Linn, 1998; Protti et al., 2005). However, other studies have shown that strychnine, in the concentrations commonly used, is also a potent competitive antagonist of α7 nicotinic acetylcholine receptors (nAChRs; Matsubayashi et al., 1998). We tested the effects of low micromolar concentrations of strychnine and 3-[2′-phosphonomethyl[1,1′-biphenyl]-3-yl] alanine (PMBA), a specific glycine receptor blocker (Saitoh et al., 1994; Hosie et al., 1999) on the activation of both α7 nAChRs on retinal ganglion cells and on ganglion cell responses to a light flash. Extracellular recordings were obtained from ganglion cells in an isolated retina/choroid preparation and 500 μM choline was used as an α7 agonist (Alkondon et al., 1997). We recorded from brisk sustained and brisk transient OFF cells, many of which have been previously shown to have α7 receptors (Strang et al., 2005). Further, we tested the effect of strychnine, PMBA and α-bungarotoxin on the binding of tetramethylrhodamine α-bungarotoxin in the inner plexiform layer. Our data indicates that strychnine, at doses as low as 1.0 μM, can inhibit the α7 nAChR-mediated response to choline, but PMBA at concentrations as high as 0.4 μM does not. Binding studies show strychnine and α-bungarotoxin inhibit binding of labeled α-bungarotoxin in the IPL. Thus, the effects of strychnine application may be to inhibit glycine receptors expressed by ganglion cell or to inhibit amacrine cell α7 nAChRs, both of which would result in an increase in the ganglion cell responses. Further research will be required to disentangle the effects of strychnine previously believed to be caused by a single mechanism of glycine receptor inhibition.
Glycine receptor subunit composition alters the action of GABA antagonists
- PING LI, MALCOLM SLAUGHTER
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- 23 July 2007, pp. 513-521
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GABA receptor antagonists produce an unexpectedly significant inhibition of native glycine receptors in retina and in α1 or α2 homomeric glycine receptors (GlyRs) expressed in HEK 293 cells. In this study we evaluate this phenomenon in heteromeric glycine receptors, formed by mixing α1, α2, and β subunits. Picrotoxinin, picrotin, SR95531, and bicuculline are all more effective antagonists at GlyRs containing α2 subunits than α1 subunits. Inclusion of β subunits reduces the inhibitory potency of picrotoxinin and picrotin but increases the potency of SR95531 and bicuculline. As a result of these two factors, bicuculline is particularly poor at discriminating GABA and glycine receptors. Picrotin, which has been reported to be inactive at GABA receptors, blocks glycine currents in retina and in HEK293 cells, suggesting its utility as a selective glycine antagonist. However, picrotin is a more potent inhibitor of GABA than glycine in retinal neurons. We also tested if GABA and glycine receptor subunits can combine to form functional receptors. If GABAAR γ2S subunits are co-expressed with GlyR α subunits, the mixed receptor is glycine-sensitive and GABA-insensitive. But the mixed receptor exhibits a non-competitive picrotoxinin inhibition that is not observed in the homomeric GlyRs. This suggests that glycine and GABA subunits can co-assemble to form functional glycine receptors.
Nicotinic acetylcholine receptor expression by directionally selective ganglion cells
- CHRISTIANNE E. STRANG, JORDAN M. RENNA, FRANKLIN R. AMTHOR, KENT T. KEYSER
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- 09 August 2007, pp. 523-533
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Acetylcholine (ACh) enhances the preferred direction responses of directionally selective ganglion cells (DS GCs; Ariel & Daw, 1982; Ariel & Adolph, 1985) through the activation of nicotinic acetylcholine receptors (nAChRs; Ariel & Daw, 1982; Massey et al., 1997; Kittila & Massey, 1997). DS GCs appear to express at least two types of nAChRs, those that are sensitive to the partially subtype-specific antagonist methyllycaconitine (MLA), and those that are MLA-insensitive (Reed et al., 2002). Our purpose was to confirm the expression of α7 nAChRs by DS GCs and to assess the contributions of other nAChR subtypes to DS GC responses. Using choline as a nAChR partially subtype-specific agonist, we found that the majority of DS GCs demonstrated responses to choline while under synaptic blockade. The blockade or reduction of choline-induced responses by bath application of nanomolar (nM) concentrations of MLA provided direct evidence that the choline responses were mediated by α7 nAChRs. Because choline is a partial agonist for α3β4 nAChRs (Alkondon et al., 1997), the residual choline responses are consistent with mediation by α3β4 nAChRs. Additionally, a subset of DS GCs responded to nicotine but not to choline, indicating the expression of a third nAChR subtype. The pharmacological results were supported by single cell reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry experiments. The expression of α7 and specific non-α7 nAChR subtypes was correlated with the preferred direction. This indicates the possibility of differential responses to ACh depending on the direction of movement. This is the first description of differential expression of multiple nAChR subtypes by DS GCs.
Amacrine cell contributions to red-green color opponency in central primate retina: A model study
- D.S. LEBEDEV, D.W. MARSHAK
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- 28 September 2007, pp. 535-547
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To investigate the contributions of amacrine cells to red-green opponency, a linear computational model of the central macaque retina was developed based on a published cone mosaic. In the model, amacrine cells of ON and OFF types received input from all neighboring midget bipolar cells of the same polarity, but OFF amacrine cells had a bias toward bipolar cells whose center responses were mediated by middle wavelength sensitive cones. This bias might arise due to activity dependent plasticity because there are midget bipolar cells driven by short wavelength sensitive cones in the OFF pathway. The model midget ganglion cells received inputs from neighboring amacrine cells of both types. As in physiological experiments, the model ganglion cells showed spatially opponent responses to achromatic stimuli, but they responded to cone isolating stimuli as though center and surround were each driven by a single cone type. Without amacrine cell input, long and middle wavelength sensitive cones contributed to both the centers and surrounds of model ganglion cell receptive fields. According to the model, the summed amacrine cell input was red-green opponent even though inputs to individual amacrine cells were unselective. A key prediction is that GABA and glycine depolarize two of the four types of central midget ganglion cells; this may reflect lower levels of the potassium chloride co-transporter in their dendrites.
Laminin deficits induce alterations in the development of dopaminergic neurons in the mouse retina
- VIKTÓRIA DÉNES, PAUL WITKOVSKY, MANUEL KOCH, DALE D. HUNTER, GERMÁN PINZÓN-DUARTE, WILLIAM J. BRUNKEN
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- 22 August 2007, pp. 549-562
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Genetically modified mice lacking the β2 laminin chain (β2null), the γ3 laminin chain (γ3 null), or both β2/γ3 chains (compound null) were produced. The development of tyrosine hydroxylase (TH) immunoreactive neurons in these mouse lines was studied between birth and postnatal day (P) 20. Compared to wild type mice, no alterations were seen in γ3 null mice. In β2 null mice, however, the large, type I TH neurons appeared later in development, were at a lower density and had reduced TH immunoreactivity, although TH process number and size were not altered. In the compound null mouse, the same changes were observed together with reduced TH process outgrowth. Surprisingly, in the smaller, type II TH neurons, TH immunoreactivity was increased in laminin-deficient compared to wild type mice. Other retinal defects we observed were a patchy disruption of the inner limiting retinal basement membrane and a disoriented growth of Müller glial cells. Starburst and AII type amacrine cells were not apparently altered in laminin-deficient relative to wild type mice. We postulate that laminin-dependent developmental signals are conveyed to TH amacrine neurons through intermediate cell types, perhaps the Müller glial cell and/or the retinal ganglion cell.
How robust is a neural circuit?
- PETER STERLING, MICHAEL FREED
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- 22 August 2007, pp. 563-571
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Design in engineering begins with the problem of robustness—by what factor should intrinsic capacity exceed normal demand? Here we consider robustness for a neural circuit that crosses the retina from cones to ganglion cells. The circuit's task is to represent the visual scene at many successive stages, each time by modulating a stream of stochastic events: photoisomerizations, then transmitter quanta, then spikes. At early stages, the event rates are high to achieve some critical signal-to-noise ratio and temporal bandwidth, which together set the information rate. Then neural circuits concentrate the information and repackage it, so that nearly the same total information can be represented by modulating far lower event rates. This is important for spiking because of its high metabolic cost. Considering various measurements at the outer and inner retina, we conclude that the “safety factors” are about 2–10, similar to other tissues.
Expression of circadian clock genes in retinal dopaminergic cells
- RONALD DORENBOS, MASSIMO CONTINI, HAJIME HIRASAWA, STEFANO GUSTINCICH, ELIO RAVIOLA
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- 17 August 2007, pp. 573-580
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The mammalian neural retina contains single or multiple intrinsic circadian oscillators that can be directly entrained by light cycles. Dopaminergic amacrine (DA) cells represent an especially interesting candidate as a site of the retinal oscillator because of the crucial role of dopamine in light adaptation, and the widespread distribution of dopamine receptors in the retina. We hereby show by single-cell, end-point RT-PCR that retinal DA cells contain the transcripts for six core components of the circadian clock: Bmal1, Clock, Cry1, Cry2, Per1, and Per2. Rod photoreceptors represented a negative control, because they did not appear to contain clock transcripts. We finally confirmed that DA cells contain the protein encoded by the Bmal1 gene by comparing immunostaining of the nuclei of DA cells in the retinas of wildtype and Bmal1−/− mice. It is therefore likely that DA cells contain a circadian clock that anticipates predictable variations in retinal illumination.
Vanilloid receptor 1 (TRPV1/VR1) co-localizes with fatty acid amide hydrolase (FAAH) in retinal amacrine cells
- SARAH ZIMOV, STEPHEN YAZULLA
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- 09 August 2007, pp. 581-591
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Fatty acid amide hydrolase (FAAH) is the degradative enzyme for anandamide (AEA), an endogenous ligand for the vanilloid receptor (TRPV1) and cannabinoid receptor 1. As FAAH and TRPV1 are integral membrane proteins, FAAH activity could modulate the availability of AEA for TRPV1 activation. Previous studies in this laboratory reported an extensive endocannabinoid system in goldfish retina. Immunocytochemistry was used to determine the relative distributions of FAAH-immunoreactivity (IR) and TRPV1-IR in goldfish retina. Here, we show the first example in an intact neural system in which TRPV1-IR co-localizes in subpopulations of FAAH-immunoreactive neurons, in this case amacrine cells. These cells are rare and consist of three subtypes: 1. ovoid cell with granular-type dendrites restricted to sublamina a, 2. pyriform cell with smooth processes in sublamina b, and 3. fusiform cell with smooth processes that project to sublaminae a and b. The varied appearances of reaction product in the dendrites suggest different subcellular localization of TRPV1, and hence function of FAAH activity regarding TRPV1 stimulation among the cell types. Ovoid and pyriform amacrine cells, but not fusiform cells, labeled with GAD-IR and constituted subsets of GABAergic amacrine cells. TRPV1 amacrine cells, though rare, are represented in the ON, OFF and ON/OFF pathways of the retina. As TRPV1 stimulation increases intracellular calcium with numerous downstream effects, co-localization of TRPV1 and FAAH suggests an autoregulatory function for anandamide. Due to the rarity of these cells, the three vanilloid amacrine cell types may be involved in global effects rather than feature extraction, for example: sampling of ambient light or maintaining homeostasis.
Dopaminergic modulation of tracer coupling in a ganglion-amacrine cell network
- STEPHEN L. MILLS, XIAO-BO XIA, HIDEO HOSHI, SALLY I. FIRTH, MARGARET E. RICE, LAURA J. FRISHMAN, DAVID W. MARSHAK
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- 22 August 2007, pp. 593-608
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Many retinal ganglion cells are coupled via gap junctions with neighboring amacrine cells and ganglion cells. We investigated the extent and dynamics of coupling in one such network, the OFF α ganglion cell of rabbit retina and its associated amacrine cells. We also observed the relative spread of Neurobiotin injected into a ganglion cell in the presence of modulators of gap junctional permeability. We found that gap junctions between amacrine cells were closed via stimulation of a D1 dopamine receptor, while the gap junctions between ganglion cells were closed via stimulation of a D2 dopamine receptor. The pairs of hemichannels making up the heterologous gap junctions between the ganglion and amacrine cells were modulated independently, so that elevations of cAMP in the ganglion cell open the ganglion cell hemichannels, while elevations of cAMP in the amacrine cell close its hemichannels. We also measured endogenous dopamine release from an eyecup preparation and found a basal release from the dark-adapted retina of approximately 2 pmol/min during the day. Maximal stimulation with light increased the rate of dopamine release from rabbit retina by 66%. The results suggest that coupling between members of the OFF α ganglion cell/amacrine cell network is differentially modulated with changing levels of dopamine.
Screening of gap junction antagonists on dye coupling in the rabbit retina
- FENG PAN, STEPHEN L. MILLS, STEPHEN C. MASSEY
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- 22 August 2007, pp. 609-618
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Many cell types in the retina are coupled via gap junctions and so there is a pressing need for a potent and reversible gap junction antagonist. We screened a series of potential gap junction antagonists by evaluating their effects on dye coupling in the network of A-type horizontal cells. We evaluated the following compounds: meclofenamic acid (MFA), mefloquine, 2-aminoethyldiphenyl borate (2-APB), 18-α-glycyrrhetinic acid, 18-β-glycyrrhetinic acid (18-β-GA), retinoic acid, flufenamic acid, niflumic acid, and carbenoxolone. The efficacy of each drug was determined by measuring the diffusion coefficient for Neurobiotin (Mills & Massey, 1998). MFA, 18-β-GA, 2-APB and mefloquine were the most effective antagonists, completely eliminating A-type horizontal cell coupling at a concentration of 200 μM. Niflumic acid, flufenamic acid, and carbenoxolone were less potent. Additionally, carbenoxolone was difficult to wash out and also may be harmful, as the retina became opaque and swollen. MFA, 18-β-GA, 2-APB and mefloquine also blocked coupling in B-type horizontal cells and AII amacrine cells. Because these cell types express different connexins, this suggests that the antagonists were relatively non-selective across several different types of gap junction. It should be emphasized that MFA was water-soluble and its effects on dye coupling were easily reversible. In contrast, the other gap junction antagonists, except carbenoxolone, required DMSO to make stock solutions and were difficult to wash out of the preparation at the doses required to block coupling in A-type HCs. The combination of potency, water solubility and reversibility suggest that MFA may be a useful compound to manipulate gap junction coupling.
Dendritic impulse collisions and shifting sites of action potential initiation contract and extend the receptive field of an amacrine cell
- AUDREY S. ROYER, ROBERT F. MILLER
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- 28 September 2007, pp. 619-634
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We evaluated the contributions of somatic and dendritic impulses to the receptive field dimensions of amacrine cells in the amphibian retina. For this analysis, we used the NEURON simulation program with a multicompartmental, multichannel model of an On-Off amacrine cell with a three-dimensional structure obtained through computer tracing techniques. Simulated synaptic inputs were evenly spaced along the dendritic branches and organized into eight annuli of increasing radius. The first set of simulations activated each ring progressively to simulate an area summation experiment, while a second approach activated each annulus individually. Both sets of simulations were done with and without the presence of Na channels in the dendrites and soma. Unexpectedly, the receptive field dimensions observed in the area summation simulations was often smaller than that predicted from the summation of the annular simulations. Collisions of action potentials moving in opposite directions in the dendrites largely accounted for this contraction in receptive field size for the area summation studies. The presence of dendritic Na channels increased the size of the receptive field beyond that achieved in their absence and allowed the physiological size of the receptive field to approximate the physical dimensions of the dendritic tree. This receptive field augmentation was the result of impulse generating ability in the dendrites which enhanced the signal observed at the soma. These simulations provide a plausible mechanistic explanation for physiological recordings from amacrine cells that show similar phenomena.
Multiple functions of cation-chloride cotransporters in the fish retina
- ANDREY V. DMITRIEV, NINA A. DMITRIEVA, KENT T. KEYSER, STUART C. MANGEL
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- 28 September 2007, pp. 635-645
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A GABA- or glycine-induced increase in Cl− permeability can produce either a depolarization or hyperpolarization, depending on the Cl− equilibrium potential. It has been shown that retinal neurons express the chloride cotransporters, Na-K-2Cl (NKCC) and K-Cl (KCC), the primary molecular mechanisms that control the intracellular Cl− concentration. We thus studied (1) the localization of these cotransporters in the fish retina, and (2) how suppression of cotransporter activity in the fish retina affects function. Specific antibodies against NKCC and KCC2 revealed that both cotransporters were expressed in the outer and inner plexiform layers, and colocalized in many putative amacrine cells and in cells of the ganglion cell layer. However, the somata of putative horizontal cells displayed only NKCC immunoreactivity and many bipolar cells were only immunopositive for KCC2. In the outer retina, application of bumetanide, a specific inhibitor of NKCC activity, (1) increased the steady-state extracellular concentration of K+ ([K+]o) and enhanced the light-induced decrease in the [K+]o, (2) increased the sPIII photoreceptor-dependent component of the ERG, and (3) reduced the extracellular space volume. In contrast, in the outer retina, application of furosemide, a specific inhibitor of KCC activity, decreased sPIII and the light-induced reduction in [K+]o, but had little effect on steady-state [K+]o. In the inner retina, bumetanide increased the sustained component of the light-induced increase in [K+]o. These findings thus indicate that NKCC and KCC2 control the [K+]o and extracellular space volume in the retina in addition to regulating GABA- and glycine-mediated synaptic transmission. In addition, the anatomical and electrophysiological results together suggest that all of the major neuronal types in the fish retina are influenced by chloride cotransporter activity.
Robust directional computation in on-off directionally selective ganglion cells of rabbit retina
- NORBERTO M. GRZYWACZ, FRANKLIN R. AMTHOR
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- 28 September 2007, pp. 647-661
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The spatial and temporal interactions in the receptive fields of On-Off directionally selective (DS) ganglion cells endow them with directional selectivity. Using a variety of stimuli, such as sinusoidal gratings, we show that these interactions make directional selectivity of the DS ganglion cell robust with respect to stimulus parameters such as contrast, speed, spatial frequency, and extent of motion. Moreover, unlike the directional selectivity of striate-cortex cells, On-Off DS ganglion cells display directional selectivity to motions not oriented perpendicularly to the contour of the objects. We argue that these cells may achieve such high robustness by combining multiple mechanisms of directional selectivity.