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At least 73 records · Page 4Linked to original sources
PubMed1988

Center-surround, orientation, and directional properties of turtle retinal horizontal cells.

The spatial transfer functions (STF) of L-type horizontal cells (HC) in turtle retina were measured using drifting sine wave grafting stimuli. Two classes of STF were identified: low-pass and band-pass. A low-pass STF corresponds to a linespread function (LSF) having an excitatory center that attenuates monotonically with distance; a band-pass STF corresponds to a LSF with an excitatory center and an inhibitory surround. Two models of the surround inhibitory mechanism, based on retinal outer plexiform layer (OPL) anatomy, are tested experimentally: surround mediated lateral inhibition and surround modulated self-inhibition. In both types, sign inverting pathways are based on GABA feedback synapses, and sign conserving pathways are based on excitatory synapses and gap junctions. Temperature variation was used to modify synaptic properties and study their effect on STF. The low frequency limb of band-pass STF was most sensitive to temperature changes; its slope increased with decreasing temperature. Synaptic properties were also manipulated pharmacologically. Cutoff frequency of low-pass STF decreased from 0.5 to 0.4 cpmm during exogenous GABA. Picrotoxin (PTX) increases upper cutoff frequency and decreases low frequency limb slope in band-pass STF. Band-pass STF of a ganglion cell (GC) has higher upper and lower cutoff frequencies than a HC in the same retinal region, which corresponds to strong spatial convergence from HC to GC. Orientation sensitivity and directional selectivity were found in some HC. Differences between major and minor response axes in orientation sensitive HC were small, ca. 2 dB; orientation differences in directionally selective HC were also small (ca. 1-2 dB) but directional asymmetry was large (ca. 10-12 dB).

Animals↗
PubMed1997

Desensitization of the GABAA receptor shifts the dynamic range of retinal horizontal cells due to light and dark adaptation.

The effects of the GABAergic pathway on the dynamic range of the light response of cone-driven horizontal cells (HCs) in the carp retina were investigated using conventional intracellular recordings and computer simulations. The amplitude of the HC responses to repetitive test flashes was altered by background illumination in control Ringer's solution, but was not changed following the application of picrotoxin or bicuculline, which suggests that GABAA receptors mediate the subsequent change in light response. This phenomenon was simulated by introducing the desensitization mechanism of the GABAA receptor into a cone-HC network model. These results suggest that desensitization of the GABAA receptor shifts the dynamic range of the HCs due to light and dark adaptation.

Adaptation, Ocular↗
PubMed1994

The effects of L-glutamate, AMPA, quisqualate, and kainate on retinal horizontal cells depend on adaptational state: implications for rod-cone interactions.

We studied the responses of isolated and intact luminosity-type horizontal cells (L-HC) in the Xenopus retina to L-glutamate (L-glu) and its analogs. Isolated L-HCs studied with whole-cell patch clamp responded to L-glu, kainate (KA), AMPA, or quisqualate (quis) with inward currents from a holding potential of -60 mV, associated with a conductance increase. The current elicited by KA was relatively large and sustained, whereas AMPA or quis evoked a desensitizing current. Coapplication of quis and KA resulted in a smaller current and conductance change than that evoked by a pulse of either alone at the same concentration. This finding suggests that the L-HC has a single subtype of glutamate receptor that responds to both quis and KA. Prior exposure to dopamine enhanced the KA-evoked current about twofold. In the superfused eyecup we found that L-HC responses to quinoxalinediones (CNQX or DNQX) and to L-glu, KA, AMPA, and quis varied as a function of adaptational state. When driven exclusively by either cones or by rods, CNQX/DNQX hyperpolarized the L-HC and reduced its light response, without altering response kinetics, indicating that both rods and cones communicate with L-HCs at ionotropic glutamatergic synapses. Under mesopic conditions, however, as CNQX or DNQX reduced cone input, the rod input to the L-HC increased up to fivefold in magnitude and had slowed kinetics. The depolarizing response of the L-HC to L-glu, AMPA, or quis was relatively small and transient under photopic conditions, but was much larger and sustained when the eyecup was dark adapted. The D1 dopamine antagonist SCH 23390 potentiated the response to quis. In contrast, responses to KA were largest in light-adapted eyecups, were potentiated by a D1 dopamine agonist, SKF 38393, and were reduced by SCH 23390. We hypothesize that the segregated populations of glutamate receptors in the L-HC opposite cone and rod synaptic endings can be separately modulated to respond differentially to the native transmitter, glutamate. In photopic and mesopic states the dominant cone input tonically inhibits rod to L-HC communication. This inhibition appears to occur at the postsynaptic membrane and may be mediated by second messengers.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1990

Renewal of electrotonic synapses in teleost retinal horizontal cells.

In teleost retinas, the somata of same-type cone horizontal cells are electrically coupled via extensive gap junctions, as are the axon terminals of same-type cells. This coupling persists throughout the animal's life and is modulated by dopamine and conditions of light- vs. dark-adaptation. Gap junction particle density in goldfish horizontal cell somata has also been shown to change under these conditions, indicating that these junctions are dynamic. We have used electron microscopy to examine gap junctions in bass horizontal cells with a fixation method that facilitates detection of gap junctions. Annular gap junction profiles were observed in the somatic cytoplasm of all cone horizontal cell types in both light- and dark-adapted animals. Serial sections showed that most profiles represented gap junction vesicles free within the cytoplasm; the remainder represented vesicles still attached to extensive plasma membrane gap junctions by a thin cytoplasmic neck, suggestive of an intermediate stage in endocytosis. Observations of gap junction vesicles containing fragments of gap junctional membrane and/or fused with lysosomal bodies further supported this hypothesis. Because gap junctions persist between the horizontal cells, we propose that gap junction endocytosis and lysosomal degradation are balanced by addition of new junctions. While endocytosis has been widely demonstrated to serve in programmed removal of gap junctions (without subsequent replacement), from both nonneuronal cells and developing neurons, this study indicates that it can also function in the renewal of electrical synapses in the adult teleost retina, where gap junction elimination is not the goal.

Animals↗
PubMed1991

Gap junction morphology of retinal horizontal cells is sensitive to pH alterations in vitro.

Isolated goldfish retinae were incubated in NaHCO3-reduced solutions, a treatment known to lower intracellular pH and to decrease gap-junction-mediated coupling between cells. The morphology of the gap junctions of horizontal cells examined by means of freeze-fracture replicas and ultrathin sections displays alterations after such treatment. The gap-junctional particles aggregate into dense clusters or crystalline arrays, whereas controls (pH 7.5) display a loose arrangement of particles. Incubation in NaHCO3-reduced solution leads to the appearance, in ultrathin sections, of prominent, electron-dense material beneath the gap-junctional membranes. Both effects, the increasing density of particles and the appearance of electron-dense material, are reversible. The application of dopamine, which uncouples horizontal cells, and its antagonist haloperidol produce less clear-cut effects on particle density in vitro.

Animals↗
PubMed1983

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

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

Amino Acids↗
PubMed1983

Carrier-mediated release of GABA from retinal horizontal cells.

H1 horizontal cells in goldfish retina are probably GABAergic and receive excitatory synaptic input from red cones. This input should affect the synaptic release of GABA from H1 cells. We studied the uptake and release of [3H]GABA from the isolated goldfish retina by use of autoradiography. When retinas were incubated in the light for 15 min in 0.72 microM [3H]GABA, heavy label was found over the somata (HS) and axon terminals (HAT) of H1 horizontal cells, and over pyriform amacrine cell bodies and their processes in sublamina b of the IPL. Postincubation of retinas, preloaded with [3H]GABA, in 0.5-10 mM L-glutamate or 0.1-10 mM L-aspartate, resulted in a dose-dependent and selective loss of [3H]GABA from HS and very little loss from HAT. This loss was not due to an efflux of metabolites of [3H]GABA or to any calcium-dependent vesicular release of [3H]GABA from HS. The glutamate-evoked release of [3H]GABA by H1 cells was sodium dependent, sensitive to substitution of lithium for sodium, and inhibited by nipecotic acid. In addition, [3H]GABA was released from HS by 0.1 mM ouabain but not by 50 mM potassium chloride. Our results suggest that the chemically evoked release of [3H]GABA from HS is mediated by a sodium-dependent transport carrier which may be responsible for the high affinity uptake of [3H]GABA by H1 cells as well. Since synaptic vesicles are not found at presumed synaptic release sites in H1 cells, we suggest that the GABA which is released synaptically from H1 cells may derive from a cytoplasmic pool of GABA and is released by means of a transport carrier. This carrier appears to depend primarily on the sodium concentration gradient across the H1 cell membrane rather than on the membrane potential of the H1 cell for its action. The relevance of the carrier-mediated release of GABA from HS in regard to the synaptic function of H1 cells is discussed.

Animals↗
PubMed1984

Responses of solitary retinal horizontal cells to L-glutamate and kainic acid are antagonized by D-aspartate.

Solitary horizontal cells dissociated from goldfish retinas depolarized when exposed to micromolar doses of either L-glutamate or kainic acid. The responses to both of these agonists were antagonized by D-aspartate, and unaffected by L-aspartate, L-glutamic acid diethyl ester and folic acid. the results of the present study thus suggest that L-glutamate and kainic acid may produce depolarizations of horizontal cells by interacting with pharmacologically similar membrane receptors.

Animals↗
PubMed1991

Characteristics of single-channels activated by quisqualate and kainate in teleost retinal horizontal cells.

There is increasing evidence in the teleost retina that the excitatory amino acid glutamate is the neurotransmitter used by some photoreceptors. Single kainate and quisqualate channels were recorded on isolated white bass horizontal cells using patch-clamp techniques. Two categories of channels were observed. The first, labelled a slow-channel, exhibited conductance and open time averages for channels activated by quisqualate of 8.5 pS and 8.8 msec, and for kainate 8.5 pS and 4.5 msec. The closed times of these channels could be described by two time constants. The second channel category was termed a fast-channel. Quisqualate and kainate activated channels in this category with two prominent conductances in the range of about 10 pS and 20-30 pS and open times of 1-2 msec. These channels demonstrated closed times with only a single time constant. Openings of slow-channels elicited by the agonists tended to occur in bursts. Activity of the fast-channels was noisy and no bursting behavior could be seen. Both channels exhibited multiple conductance states.

Animals↗
PubMed1982

Depolarization of retinal horizontal cells by excitatory amino acid neurotransmitter agonists.

We have recorded the intracellular membrane potential of horizontal cells, second-order interneurones of the vertebrate retina, from fish retinae perfused with Ringer solution containing agonist drugs of the excitatory neurotransmitters, L-glutamate and L-aspartate. We show that at concentrations greater than about 10 microM, kainate and quisqualate have a potent depolarizing effect on horizontal cells and suppress their light evoked electrical responses (S-potentials). In contrast, a third agonist, N-methyl-D-aspartate, hyperpolarizes horizontal cells. The depolarizing action of kainate and quisqualate persists in the presence of the synaptic blocker, cobalt chloride, which implies that they bind directly on the horizontal cell membranes. Two kainate-related drugs, which are active on invertebrate neurones, were also examined, one, alpha-ketokainate, simulates the action of kainate, but the other, dihydrokainate, is ineffective on horizontal cells. L-Glutamate binds with high affinity at quisqualate sites, whereas L-aspartate binds with high affinity at NMDA sites, thus we conclude that L-glutamate is the likely neurotransmitter at the photoreceptor-horizontal cell synapse.

Amino Acids↗
PubMed1982

Selective potentiation of retinal horizontal cell responses to L-glutamate by D-aspartate.

1. L-Glutamate and L-aspartate depolarize type H1 horizontal cells in the isolated retina of goldfish, but only at millimolar concentrations. 2. When applied in the presence of D-aspartate, L-glutamate depolarizes H1 cells at concentrations nearly 15-fold lower than when it is applied alone. The effects of L-aspartate were not potentiated by either D-aspartate or D-glutamate. 3. Since D-aspartate seems also to enhance the effect of the transmitter released by cone photoreceptors, these results are consistent with the possibility that L-glutamate is a neurotransmitter of cones.

Animals↗
PubMed1996

Protein kinase C does not mediate the dopamine-dependent modulation of glutamate receptors in retinal horizontal cells of the perch (Perca fluviatilis).

The whole-cell patch-clamp technique was employed to record membrane currents from cultured horizontal cells of the perch (Perca fluviatilis). The cells were voltage clamped and slowly superfused with an extracellular solution containing L-glutamate. The glutamate concentration in the bath was continuously measured with the help of photodiode and a dye which accumulated in the bath together with the agonist. The PKA-activator forskolin mimicked the effect of dopamine and enhanced glutamate-induced currents, while application of the PKC stimulator PMA or the synthetic diacylglycerol analogue OAG had no significant effects on the dose-response curves of glutamate induced-currents. These results may indicate that the modulation of glutamate receptors in fish horizontal cells is not mediated via a PKC-dependent pathway.

Animals↗
PubMed1996

Use-dependent and use-independent blocking actions of picrotoxin and zinc at the GABAC receptor in retinal horizontal cells.

The inhibitory actions of picrotoxin (PTX) and zinc on the GABAC receptor in acutely isolated catfish cone horizontal cells were studied and compared using the whole-cell patch clamp technique. PTX blocked the GABAC current elicited by 30 microM GABA with IC50 = 0.64 microM. Over a PTX concentration range of 1-100 microM, simultaneous application of PTX with GABA (30 microM) produced current transients at both the onset and offset of the drug pulse. When the PTX concentration was maintained before, during, and after GABA application, the current transients at the onset and offset of GABA application disappeared. Thus, these transients seem to reflect a slower initial action of PTX at, and faster washout of PTX from, the GABAC receptor than GABA when they were co-applied. The full recovery from PTX inhibition required a second GABA application. Recovery could not be achieved by a prolonged wash in the absence of GABA. These results suggest that PTX effect is use-dependent. Zinc also potently blocked the GABAC current elicited by 30 microM GABA with an IC50 about an order of magnitude higher than that of PTX (IC50 = 8.2 microM). However, only the onset, but not the offset current transient was observed when zinc was simultaneously applied with GABA. The full recovery of the GABAC current from zinc inhibition was obtained after washing for 20 sec and did not require a subsequent GABA application. This indicates that the zinc effect is use-independent. Our findings suggest that: (1) the zinc binding site is on the surface of the GABAC receptor molecule; (2) there is a PTX binding site that is probably inside the receptor and its access requires GABA binding to the receptor.

Animals↗
PubMed1997

Nitric oxide, 2-amino-4-phosphonobutyric acid and light/dark adaptation modulate short-wavelength-sensitive synaptic transmission to retinal horizontal cells.

Light-induced changes in the input resistance (Rin) of external, luminosity (i.e. H1) type horizontal cell (HC) perikarya were studied by the bridge-balance method in light-adapted and dark-adapted retinae of carp. Changes in input resistance (delta Rin) induced by short-(460 nm) and long-wavelength (674 nm) flashes, adjusted in intensity to elicit equal-amplitude membrane voltage responses (equal-voltage condition), were measured. In light-adapted retinae, long-wavelength stimuli increased Rin consistently; in contrast, the increase was much less with short-wavelength stimuli. This equal-voltage chromatic delta Rin difference was lost in dark-adapted retinae whereby the delta Rin (an increase) became the same for short- and long-wavelengths. The chromatic delta Rin difference could be recovered by light adaptation or application of sodium nitroprusside to the dark-adapted retinae. Conversely, the equal-voltage chromatic delta Rin difference was eliminated by injection of NG-monomethyl-L-arginine into H1HCs of the light-adapted retinae or by treating the retinae with 2-amino-4-phosphonobutyrate (APB). These results suggest that H1HCs of the carp retina possess distinct postsynaptic mechanisms which mediate short- and long-wavelength signal transmission. Furthermore, it appears that the short-wavelength-sensitive pathway is active only during the light-adapted state of the retina. Taken together, therefore, the short-wavelength transmission to H1HCs probably operates on an APB-sensitive glutamate receptor, with nitric oxide as a light-adaptive messenger.

Acclimatization↗