scholarly journals Lateral feedback from monophasic horizontal cells to cones in carp retina. I. Experiments.

1989 ◽  
Vol 93 (4) ◽  
pp. 681-694 ◽  
Author(s):  
M Kamermans ◽  
B W van Dijk ◽  
H Spekreijse ◽  
R C Zweypfenning

The spatial and color coding of the monophasic horizontal cells were studied in light- and dark-adapted retinae. Slit displacement experiments revealed differences in integration area for the different cone inputs of the monophasic horizontal cells. The integration area measured with a 670-nm stimulus was larger than that measured with a 570-nm stimulus. Experiments in which the diameter of the test spot was varied, however, revealed at high stimulus intensities a larger summation area for 520-nm stimuli than for 670-nm stimuli. The reverse was found for low stimulus intensities. To investigate whether these differences were due to interaction between the various cone inputs to the monophasic horizontal cell, adaptation experiments were performed. It was found that the various cone inputs were not independent. Finally, some mechanisms for the spatial and color coding will be discussed.

1996 ◽  
Vol 76 (3) ◽  
pp. 2005-2019 ◽  
Author(s):  
W. A. Hare ◽  
W. G. Owen

1. It is widely believed that signals contributing to the receptive field surrounds of retinal bipolar cells pass from horizontal cells to bipolar cells via GABAergic synapses. To test this notion, we applied gamma-aminobutyric acid (GABA) agonists and antagonists to isolated, perfused retinas of the salamander Ambystoma tigrinum while recording intracellularly from bipolar cells, horizontal cells, and photoreceptors. 2. As we previously reported, administration of the GABA analogue D-aminovaleric acid in concert with picrotoxin did not block horizontal cell responses or the center responses of bipolar cells but blocked the surround responses of both on-center and off-center bipolar cells. 3. Surround responses were not blocked by the GABA, antagonists picrotoxin or bicuculline, the GABAB agonist baclofen or the GABAB antagonist phaclofen, and the GABAC antagonists picrotoxin or cis-4-aminocrotonic acid. Combinations of these drugs were similarly ineffective. 4. GABA itself activated a powerful GABA uptake mechanism in horizontal cells for which nipecotic acid is a competitive agonist. It also activated, both in horizontal cells and bipolar cells, large GABAA conductances that shunted light responses but that could be blocked by picrotoxin or bicuculline. 5. GABA, administered together with picrotoxin to block the shunting effect of GABAA activation, did not eliminate bipolar cell surround responses at concentrations sufficient to saturate the known types of GABA receptors. 6. Surround responses were not blocked by glycine or its antagonist strychnine, or by combinations of drugs designed to eliminate GABAergic and glycinergic pathways simultaneously. 7. Although we cannot fully discount the involvement of a novel GABAergic synapse, the simplest explanation of our findings is that the primary pathway mediating the bipolar cell's surround is neither GABAergic nor glycinergic.


1996 ◽  
Vol 76 (4) ◽  
pp. 2307-2315 ◽  
Author(s):  
D. G. McMahon ◽  
L. V. Ponomareva

1. In the retina, as in other regions of the vertebrate central nervous system, glutamate receptors mediate excitatory chemical synaptic transmission and are a critical site for the regulation of cellular communication. In this study, retinal horizontal cells from the hybrid less were dissociated in cell culture, voltage clamped by the whole cell recording technique, and the currents evoked by application of excitatory amino acids recorded. 2. Responses to glutamate and its agonist kainate were reduced by approximately 50% in the presence of the nitric oxide (NO) donors sodium nitroprusside and S-nitroso-N-acetylpenicillamine. The effect of these compounds was blocked by the NO scavenger hemoglobin. 3. This effect of NO donors on kainate currents could be mimicked by the application of a membrane permeable guanosine 3',5'-cyclic monophosphate (cGMP) analogue, 8-Br-cGMP. The NO effect was also blocked by application of the guanylate cyclase inhibitor LY-83583, and by a protein kinase G inhibitor peptide. 4. In H1-type horizontal cells, stimulation of endogenous nitric oxide synthase with L-arginine reduced kainate responses, whereas application of D-arginine had no effect. 5. This receptor modulation mechanism may act in concert with other pre- and postsynaptic mechanisms to modify horizontal cell synaptic function according to the adaptational state of the retina and also may protect horizontal cells from glutamate excitotoxicity.


1997 ◽  
Vol 14 (2) ◽  
pp. 207-212 ◽  
Author(s):  
Keith M. Studholme ◽  
Stephen Yazulla

AbstractThere are four types of horizontal cell in the goldfish retina, three cone- and one rod-type. The neurotransmitter of only one type, the H1 (cone) horizontal cell, has been identified as GABA. 3H-adenosine uptake was examined as a possible marker for the other classes of horizontal cell. Isolated goldfish retinae were incubated in 3H-adenosine (10–40 μCi) in HEPES-buffered saline for 30 min, then fixed, embedded in plastic, and processed for light-microscopic autoradiography (ARG). For double-label immuno/ARG studies, l-μm-thick sections were processed for GABA postembed immunocytochemistry, then for ARG. 3H-adenosine uptake was localized to cone photoreceptors, presumed precursor cells in the proximal outer nuclear layer, and to a single, continuous row of horizontal cell bodies in the inner nuclear layer. No uptake was localized to the region of horizontal cell axon terminals. 3H-adenosine uptake did not colocalize with GABA-IR in H1 horizontal cells, but it did colocalize with adenosine deaminase immunoreactivity. It is concluded that 3H-adenosine uptake selectively labels rod horizontal cells in the goldfish retina based on position and staining pattern, which are similar to rod horizontal cells stained by Golgi or HRP injection methods. The use of 3H-adenosine uptake may provide a useful tool to study other properties of rod horizontal cells (i.e. development) as well as provide clues as to the transmitter used by these interneurons.


1991 ◽  
Vol 66 (6) ◽  
pp. 1993-2001 ◽  
Author(s):  
S. Borges ◽  
M. Wilson

1. The effects of glycine on horizontal cells have been examined by microelectrode recording from superfused retinas isolated from the salamander. 2. Low concentrations of glycine (less than 50 microM) hyperpolarized horizontal cells and increased the magnitude of their light responses. Millimolar concentrations produced the opposite effect of depolarizing these cells and reducing their light response amplitudes. 3. In the presence of Co2+ and Mg2+ at concentrations sufficient to suppress the light response, millimolar glycine still exerted a depolarizing effect on horizontal cells, implying that this effect was largely a direct one on horizontal cell membranes. 4. Although both the rod and the cone contributions to horizontal cell light responses were reduced by millimolar glycine, rod input was reduced more, suggesting that millimolar glycine may also exert a presynaptic effect. 5. Strychnine (10 microns) antagonized the effects of millimolar glycine and, in the absence of exogenously applied glycine, caused horizontal cells to hyperpolarize and their light responses to increase in amplitude. This result implies that, in darkness, glycine is tonically released onto horizontal cells and maintains them in a state of partial depolarization. 6. The low-concentration effect of glycine was accompanied by an increased membrane resistance and receptive field size but no change in the balance of rod and cone input. 7. Low concentrations of glycine were often seen to cause a speeding of light responses, whereas high concentrations sometimes caused a slowing of response kinetics. Response kinetics were found to correlate with horizontal cell dark membrane potential so that, positive to -30 mV, depolarization slowed responses whereas kinetics at more negative values were largely independent of voltage.


1990 ◽  
Vol 64 (1) ◽  
pp. 248-261 ◽  
Author(s):  
R. L. Winslow ◽  
S. Ma

1. We have previously presented a model of horizontal-cell soma isolated from fish retina. The model consists of a synaptic conductance representing input from photoreceptors in parallel with voltage-dependent membrane currents. Membrane-current models are based on I-V curves measured in isolated fish horizontal cells. Bifurcation theory was used to analyze model properties. The major findings of this study were 1) the inward Ca2+ current must be inactivated to account for horizontal-cell resting potentials and hyperpolarizing responses to light stimuli in a background of dark, and 2) the synaptic conductance controls the bifurcation structure of the model, with bistable behavior occurring at small and monostable behavior occurring at larger values of the synaptic conductance. The synaptic conductance at the point of transition from bistable to monostable behavior corresponds to the activation of as few as 100 synaptic channels. Thus tonic synaptic input from photoreceptors and inactivation of the inward Ca2+ current act to “linearize” responses of isolated horizontal-cell models. 2. The model described in this paper extends these analyses to large networks of horizontal cells in which each cell is coupled resistively to its nearest neighbors and is modeled with the use of the full complement of nonlinear membrane currents. Network responses to arbitrary patterns of conductance change (simulating inputs from photoreceptors), current-, or voltage-clamp stimuli are computed using the Newton iteration. The Newton descent direction is computed using either conjugate gradient (CG) or preconditioned CG algorithms. 3. An analysis of network stability properties is performed. Network I-V curves are computed by voltage-clamping the center node and computing the current required to maintain the clamp voltage. Computations are performed on networks of model cells in which the Ca2+ current is fully activated and the synaptic conductance is zero, thus making each cell as nonlinear as possible. Coupling conductance values slightly greater than 100 pS provide a current shunt sufficient to prevent the generation of Ca2+ action potentials in the network. This coupling conductance corresponds to the conductance of as few as two gap-junction channels and is more than two orders of magnitude less than the coupling known to exist between pairs of cultured horizontal cells.(ABSTRACT TRUNCATED AT 400 WORDS)


1991 ◽  
Vol 66 (6) ◽  
pp. 2002-2013 ◽  
Author(s):  
T. A. Gilbertson ◽  
S. Borges ◽  
M. Wilson

1. Horizontal cells, identified by their morphology, were isolated from the salamander retina and examined in whole cell patch clamp. 2. All cells showed large outward currents activating positive to about -50 mV, and a minority of cells showed fast, tetrodotoxin-suppressible Na+ currents. Slow inward currents that might shape the light responses were never observed. 3. All cells showed conductance increases to both gamma-aminobutyric acid (GABA) and glycine that were completely blocked by bicuculline and strychnine, respectively. No cross-blocking by these antagonists was observed. Partial replacements of Cl- with large, impermeant anions indicated that both GABA- and glycine-evoked currents were carried by Cl- ions. 4. Responses to both GABA and glycine desensitized strongly with time constants of approximately 2 s. 5. Responses to glutamate were not enhanced by glycine. Similarly, responses to GABA were not enhanced by glutamate. 6. GABA-mediated synaptic interactions between horizontal cells may account for the changes in the kinetics of horizontal cell light responses seen when glycine is applied to the intact retina.


1987 ◽  
Vol 57 (3) ◽  
pp. 645-659 ◽  
Author(s):  
S. C. Massey ◽  
R. F. Miller

Intracellular recordings were obtained from horizontal cells in the superfused retina-eyecup preparation of the rabbit. Rod- and cone-dominated horizontal cells were studied using bath-applied excitatory amino acid analogues. Cone-dominated horizontal cell somas were depolarized by kainate (KA) or quisqualate (QQ) and their light responses were reduced or abolished. They were not affected by N-methyl-DL-aspartate (NMDLA) at concentrations up to 2 mM or by 2-amino-4-phosphonobutyrate (APB), a selective agonist for the ON bipolar cell. When synaptic transmission was blocked with cobalt, horizontal cell somas were hyperpolarized. Under these conditions, KA and QQ caused large depolarizations suggesting that these agents have a direct action on horizontal cell somas. Excitatory amino acid antagonists such as cis-2,3-piperidine dicarboxylic acid (PDA) and kynurenic acid (Kyn) hyperpolarized horizontal cell somas to the level of the light-driven membrane potential. These antagonists blocked both the light-driven responses and the depolarizing action of KA. The specific NMDA antagonist 2-amino-7-phosphonoheptanoate (AP-7) had no effect on the membrane potential or light-driven responses of horizontal cell somas. In contrast to a previous report, we found no evidence that low concentrations of NMDLA could hyperpolarize horizontal cells or act as a KA antagonist in the rabbit retina. Rod-dominated axon terminals were identified by waveform, threshold, and the presence of a large rod after-potential evoked by high light intensity. These cells were depolarized by KA and their light responses were attenuated. NMDLA and APB had no effect on these cells. The general antagonists, PDA and Kyn, hyperpolarized axon terminals and blocked their light-evoked responses. The specific NMDA antagonist, AP-7, had no effect on these cells. These results suggest that the synaptic receptors that mediate light input to both rod- and cone-dominated horizontal cells are kainate or quisqualate receptors. This implies that the rod and cone transmitters of the rabbit retina are similar, with the characteristics of an excitatory amino acid, such as glutamate.


1998 ◽  
Vol 79 (1) ◽  
pp. 190-196 ◽  
Author(s):  
Lubor Gaal ◽  
Botond Roska ◽  
Serge A. Picaud ◽  
Samuel M. Wu ◽  
Robert Marc ◽  
...  

Gaal, Lubor, Botond Roska, Serge A. Picaud, Samuel M. Wu, Robert Marc, and Frank S. Werblin. Postsynaptic response kinetics are controlled by a glutamate transporter at cone photoreceptors. J. Neurophysiol. 79: 190–196, 1998. We evaluated the role of the sodium/glutamate transporter at the synaptic terminals of cone photoreceptors in controlling postsynaptic response kinetics. The strategy was to measure the changes in horizontal cell response rate induced by blocking transporter uptake in cones with dihydrokainate (DHK). DHK was chosen as the uptake blocker because, as we show through autoradiographic uptake measurements, DHK specifically blocked uptake in cones without affecting uptake in Mueller cells. Horizontal cells depolarized from about −70 to −20 mV as the exogenous glutamate concentration was increased from ∼1 to 40 μM, so horizontal cells can serve as “glutamate electrodes” during the light response. DHK slowed the rate of hyperpolarization of the horizontal cells in a dose-dependent way, but didn't affect the kinetics of the cone responses. At 300 μM DHK, the rate of the horizontal cell hyperpolarization was slowed to only 17 ± 8.5% (mean ± SD) of control. Translating this to changes in glutamate concentration using the slice dose response curve as calibration in Fig. 2 , DHK reduced the rate of removal of glutamate from ∼0.12 to 0.031 μM/s. The voltage dependence of uptake rate in the transporter alone was capable of modulating glutamate concentration: we blocked vesicular released glutamate with bathed 20 mM Mg2+ and then added 30 μM glutamate to the bath to reestablish a physiological glutamate concentration level at the synapse and thereby depolarize the horizontal cells. Under these conditions, a light flash elicited a 17-mV hyperpolarization in the horizontal cells. When we substituted kainate, which is not transported, for glutamate, horizontal cells were depolarized but light did not elicit any response, indicating that the transporter alone was responsible for the removal of glutamate under these conditions. This suggests that the transporter was both voltage dependent and robust enough to modulate glutamate concentration. The transporter must be at least as effective as diffusion in removing glutamate from the synapse because there is only a very small light response once the transporter is blocked. The transporter, via its voltage dependence on cone membrane potential, appears to contribute significantly to the control of postsynaptic response kinetics.[Figure: see text]


1999 ◽  
Vol 115 (1) ◽  
pp. 3-16 ◽  
Author(s):  
D.A. Kraaij ◽  
H. Spekreijse ◽  
M. Kamermans

Cones in the vertebrate retina project to horizontal and bipolar cells and the horizontal cells feedback negatively to cones. This organization forms the basis for the center/surround organization of the bipolar cells, a fundamental step in the visual signal processing. Although the surround responses of bipolar cells have been recorded on many occasions, surprisingly, the underlying surround-induced responses in cones are not easily detected. In this paper, the nature of the surround-induced responses in cones is studied. Horizontal cells feed back to cones by shifting the activation function of the calcium current in cones to more negative potentials. This shift increases the calcium influx, which increases the neurotransmitter release of the cone. In this paper, we will show that under certain conditions, in addition to this increase of neurotransmitter release, a calcium-dependent chloride current will be activated, which polarizes the cone membrane potential. The question is, whether the modulation of the calcium current or the polarization of the cone membrane potential is the major determinant for feedback-mediated responses in second-order neurons. Depolarizing light responses of biphasic horizontal cells are generated by feedback from monophasic horizontal cells to cones. It was found that niflumic acid blocks the feedback-induced depolarizing responses in cones, while the shift of the calcium current activation function and the depolarizing biphasic horizontal cell responses remain intact. This shows that horizontal cells can feed back to cones, without inducing major changes in the cone membrane potential. This makes the feedback synapse from horizontal cells to cones a unique synapse. Polarization of the presynaptic (horizontal) cell leads to calcium influx in the postsynaptic cell (cone), but due to the combined activity of the calcium current and the calcium-dependent chloride current, the membrane potential of the postsynaptic cell will be hardly modulated, whereas the output of the postsynaptic cell will be strongly modulated. Since no polarization of the postsynaptic cell is needed for these feedback-mediated responses, this mechanism of synaptic transmission can modulate the neurotransmitter release in single synaptic terminals without affecting the membrane potential of the entire cell.


1999 ◽  
Vol 16 (5) ◽  
pp. 801-809 ◽  
Author(s):  
SILKE HAVERKAMP ◽  
WOLFGANG MÖCKEL ◽  
JOSEF AMMERMÜLLER

Electrophysiologically, color-opponent retinal bipolar cells respond with opposite polarities to stimulation with different wavelengths of light. The origin of these different polarities in the same bipolar cell has always been a mystery. Here we show that an intracellularly recorded and HRP-injected, red-ON, blue/green-OFF bipolar cell of the turtle retina made invaginating (ribbon associated) synapses exclusively with L-cones. Non-invaginating synapses resembling wide-cleft basal junctions were made exclusively with M-cones. Input from S-cones was not seen. From these results we suggest sign-inverting transmission from L-cones at invaginating synapses via metabotropic glutamate receptors, and sign-conserving transmission from M-cones at wide-cleft basal junctions via ionotropic receptors. To explain the pronounced blue sensitivity of the bipolar cell, computer simulations were performed using a sign-conserving input from a yellow/blue chromaticity-type (H3) horizontal cell. The response properties of the red-ON, blue/green-OFF bipolar cell could be quantitatively reproduced by this means. The simulation also explained the asymmetry in L- and M-cone inputs to the bipolar cell as found in the ultrastructural analysis and assigned a putative role to H3 horizontal cells in color processing in the turtle retina.


Sign in / Sign up

Export Citation Format

Share Document