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At least 109 records · Page 6Linked to original sources
PubMed1985

Permeability changes induced by L-glutamate in solitary retinal horizontal cells isolated from Carassius auratus.

Solitary horizontal cells isolated from goldfish retinae are depolarized by L-glutamate (Glu) (Ishida, Kaneko & Tachibana, 1984), a possible candidate for the transmitter of photoreceptors. The underlying mechanisms were analysed under voltage-clamp conditions using 'giga-seal' suction pipettes in the whole-cell recording configuration. Glu induced an inward current at the resting membrane potential (ca. -57 mV). Membrane depolarization decreased the amplitude of Glu-induced current and reversed its polarity to outward beyond approximately -3 mV. Membrane hyperpolarization below the resting potential decreased the amplitude of the Glu-induced inward current. When a K current through the anomalous rectifier, which is activated by membrane hyperpolarization (Tachibana, 1983), was blocked by Cs ions, this phenomenon disappeared and the Glu-induced current increased in amplitude with hyperpolarization. Mg ions had no effect on the reduction of the Glu-induced current at hyperpolarized potentials. It was strongly suggested that Glu produced two types of conductance change; a conductance increase due to an activation of Glu channels and a conductance decrease due to a blockage of the K current through the anomalous rectifier. The latter effect is analysed in detail in the following paper (Kaneko & Tachibana, 1985b). The Glu-activated channel was permeable to cations (Na, K, Ca, Mg, Tris and choline ions) with low selectivity, but not to anions. The least effective dose of Glu was less than 10 microM. The relation between the Glu-induced current and the membrane potential curved upwards near the reversal potential, and this relation was not affected by Mg ions.

Action Potentials↗
PubMed1986

Interaction between the soma and the axon terminal of retinal horizontal cells in Cyprinus carpio.

Intracellular recordings were made from the monophasic horizontal cells of the carp retina which are known to respond with a sustained hyperpolarization to all visible monochromatic light. The receptive field of each subcellular structure, the soma and the axon terminal, was determined using a long narrow slit of light. Somata and axon terminals showed receptive fields that encompassed almost the entire retina. This observation suggests that each aggregate of the subcellular parts forms a synctial structure. However, with increasing distance from the slit, the response peak decayed more steeply in somata than in axon terminals. The spatial decline of the peak consisted of two exponential functions in somata, while a single exponential function in axon terminals. The length constant of the axon terminal was similar to the larger length constant revealed in the soma. This finding suggests an electrical communication at work between the soma and the axon terminal. A quantitative account was made in light of a discrete resistive network model which consists of a pair of syncytia coupled through connecting axons; one represents the contiguous layer of somata and the other the contiguous layer of axon terminals. Relevant response properties computed from the model analysis were in satisfactory agreement with experimental data. It was concluded that the soma and the axon terminal of the horizontal cell are electrically connected in the cyprinid retina.

Animals↗
PubMed1983

Vasoactive intestinal peptide alters membrane potential and cyclic nucleotide levels in retinal horizontal cells.

Vasoactive intestinal peptide stimulated the synthesis of adenosine 3',5'-monophosphate in fractions of isolated carp horizontal cells. When applied extracellularly to isolated and cultured horizontal cells, the peptide also induced a slow depolarization (30 to 40 millivolts) accompanied by a decrease in membrane resistance. However, analogs of adenosine 3',5'-monophosphate applied extracellularly or intracellularly, and forscolin applied extracellularly, had no effect on the membrane potential of cultured horizontal cells, indicating that the induced depolarization was not related to the accumulation of adenosine 3',5'-monophosphate in these cells.

Animals↗
PubMed1988

The axon terminal of goldfish retinal horizontal cells: a low membrane conductance measured in solitary preparations and its implication to the signal conduction from the soma.

1. Mechanical dissociation of the enzyme-treated goldfish retina yielded somata and axon terminals of horizontal cells. The membrane properties of these solitary axon terminals were investigated using the whole-cell patch-clamp technique. 2. Axon terminals had a large input resistance, comparable to the seal resistance (approximately 30 G omega). Most axon terminals (greater than 80%) showed a nearly linear current-voltage relation between -60 and +10 mV, where the slope conductance was as small as 5 muS/cm2. Some axon terminals showed a shallow negative slope conductance in the same potential range. 3. The membrane current consisted of two components: transient and sustained. The transient component was carried by sodium ions, and the sustained component was a mixture of calcium and potassium currents. The sodium current (INa) was activated by depolarization of beyond -45 mV and was maximal (approximately 60 pA) at -10 mV. It was blocked by 5 microM tetrodotoxin and disappeared in Na+-free medium. The maximum amplitude of INa was less than 10% of INa of the soma. 4. A small calcium current (less than 6 pA) was isolated in a small proportion of cells, with an amplitude approximately 5% of the calcium current evoked in the soma under the identical recording conditions. 5. A small amount of potassium current through the anomalous rectifier was induced in the axon terminal when the membrane potential was below -60 mV. Its conductance was 15-20 muS/cm2, only 1/20 of the estimate in the soma. Other types of potassium currents were not detected. 6. It is concluded that the soma and the axon terminal have a similar set of membrane currents, but the specific membrane conductance of the axon terminal is extremely low. The signal conductivity from soma to axon terminal was assessed using a passive cable model together with numerical values obtained from the present experiments. Although the membrane conductance of the connecting axon was not measurable directly, the calculation strongly suggests that low conductance of the axon terminal membrane minimizes the leakage of signals arriving electrotonically through the thin connecting axon, even if the membrane conductance of the axon was overestimated as being identical to the soma membrane. 7. These results can explain why light-evoked responses recorded from the axon terminal are similar in amplitude as well as in waveform to those recorded from the soma, despite the lack of direct inputs from photoreceptors.

Animals↗
PubMed1988

Local superfusion modifies the inward rectifying potassium conductance of isolated retinal horizontal cells.

1. Horizontal cells were enzymatically and mechanically dissociated from the white perch (Roccus americana) retina and voltage clamped using patch electrodes. Steady-state current-voltage (I-V) relationships of solitary horizontal cells were determined by changing the membrane potential in a rampwise fashion. 2. The I-V curve of cells bathed in normal Ringer solution exhibited a large conductance increase at negative membrane potentials. This conductance activated near the K+ equilibrium potential, had no clear reversal potential, was enhanced by raising the extracellular concentration of K+, and was suppressed by external Cs+. These properties identify the conductance as the inward (anomalous) rectifier. 3. Continuous superfusion of the cells' local environment with drug-free Ringer reduced the magnitude of the inward rectifier current and shifted its activation point to more negative potentials. This effect developed over approximately 30 s, lasted as long as superfusion continued and was reversible upon cessation of superfusion. 4. Pressure ejection of drug-free Ringer solution onto cells bathed in the identical solution also reduced the magnitude of the inward rectifier current, although the effects were more rapid and more transient than those exerted by superfusion. Pressure ejection had little effect when cells were simultaneously superfused with Ringer, suggesting a common mode of action on the inward rectifier. 5. In the absence of superfusion, pressure ejection of Ringer containing 200 microM L-glutamate had a biphasic effect on membrane conductance. At potentials above -60 mV, glutamate caused a conductance increase with a reversal potential near +10 mV. At potentials below -60 mV, glutamate caused a conductance decrease whose reversal potential could not reliably be determined. The latter effect was similar to the suppression of the inward rectifier by application of Ringer alone, suggesting that it may represent an artifact of pressure ejection rather than a direct effect of glutamate. 6. In support of this interpretation, we found that pressure ejection of glutamate in the presence of external Cs+ (which blocks the inward rectifier) or during local superfusion with Ringer (which prevents attenuation of the inward rectifier by pressure ejection) did not cause a conductance decrease at negative potentials. Under these conditions, glutamate caused primarily a conductance increase with a reversal potential near +10 mV.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Bifurcation analysis of nonlinear retinal horizontal cell models. II. Network properties.

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)

Animals↗
PubMed1991

Depolarizing actions of GABA and glycine on amphibian retinal horizontal cells.

1. The effects of inhibitory amino acid transmitters on horizontal cells in the superfused amphibian retina were studied by the use of conventional intracellular recording techniques. 2. Gamma-aminobutyric acid (GABA) caused a calcium-independent depolarization of horizontal cells in mud puppy and tiger salamander. This action was mimicked by muscimol but not baclofen (BAC) and blocked by bicuculline and picrotoxin (PTX), matching the GABAa receptor profile. 3. The purported GABA uptake inhibitors nipecotate (NPA) and guvacine (GUV) acted as GABAa agonists, having pharmacological properties very similar to GABA itself. These agents also activated receptors of amacrine and ganglion cells, causing membrane polarizations similar to GABA. Concentrations of these analogues that did not activate the GABAa receptor (submillimolar) did not lower the effective dose of GABA, even after prolonged application. 4. Glycine (GLY) also depolarized horizontal cells, but only in approximately 25% of the horizontal cells was the amplitude of the depolarization as great as GABA. The glycine response was blocked by both strychnine (STR, 10 microM) and PTX (100 microM). In contrast, the action of GABA was unaffected by STR. 5. Ion substitution and channel-blocking agents indicated that the effects of applied GABA and GLY were independent of both external sodium and calcium. 6. The results suggest that GABA receptors on horizontal cells may act 1) as a positive feedback system to modulate the light response and 2) as a mechanism for chemical coupling between horizontal cells.

Animals↗
PubMed1996

Activation of NMDA receptors produces dopamine-mediated changes in fish retinal horizontal cell light responses.

1. The action of N-methyl-D-aspartate (NMDA) on cone horizontal cells was studied in in vitro goldfish retinas superfused with a bicarbonate-based Ringer solution that contained D-serine (0.5 microM), a glycine analogue, but no added Mg2+. Horizontal cell light responses and electrical coupling were assessed by monitoring responses to full-field stimuli and to small, centered (0.4 mm diam) spots of light, respectively. 2. NMDA uncoupled horizontal cells, reduced their light responsiveness, and acted in a dose-dependent manner, with threshold at 10 microM and maximum effect at 100 microM. 3. Application of the NMDA antagonists DL-2-amino-7-phosphonoheptanoic acid-AP-5) or D-2-amino-5-phosphonopentanoic acid-AP-5) (50 microM) blocked the uncoupling action of NMDA (100 microM), as did prior application of SCH23390, a dopamine D1 antagonist, or prior treatment of the retinas with 6-hydroxydopamine, a procedure that destroys dopaminergic neurons. 4. Addition of Mg2+ (1 mM) partially blocked the effects of NMDA at 100 microM and completely blocked the effects of 50 microM NMDA. The effects of NMDA (50 or 100 microM) were also reduced if it was applied without D-serine. 5. Both flickering (5 Hz) and sustained light stimulation uncoupled horizontal cells and reduced their light responsiveness. Application of AP-7 blocked the effects of flickering light stimulation, but did not block the effects of sustained light. 6. These results suggest that activation of NMDA receptors in the fish retina uncouples cone horizontal cells and decreases their light responsiveness by increasing dopamine release. The results further suggest that flickering light, but not sustained light, increases the release of dopamine through activation of NMDA receptors.

Animals↗
PubMed1998

Multiple second-messenger system modulation of voltage-activated calcium currents in teleost retinal horizontal cells.

Two voltage-activated calcium currents, a transient T-type and a PL-sustained type, have been measured in isolated, cultured white bass horizontal cells. These two voltage-activated calcium currents were found to be modulated by two independent second-messenger systems. Furthermore, activation of either second-messenger system led to similar changes in calcium current activity. Activation of the cyclic AMP second-messenger pathway or the sn-1,2-diacylglycerol (DAG) second-messenger system resulted in a significant decrease in the amplitude of the transient current and a simultaneous large increase in the amplitude of the sustained current. Both second-messenger systems achieved their effects through protein phosphorylation. The cyclic AMP pathway resulted in the activation of protein kinase A (PKA) and the DAG pathway worked to activate protein kinase C (PKC). Two protein kinase inhibitors were analyzed in this study for their ability to inhibit second-messenger activated protein kinase activity and separate the two pathways. The peptide cyclic AMP-dependent protein kinase inhibitor and staurosporine were found to be nonspecific at high concentrations and inhibited both second-messenger pathways. At low concentrations however, staurosporine specifically inhibited only PKC, whereas adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase inhibitor was selective for PKA. Both second-messenger systems were activated by the neuromodulator, dopamine. Thus one agonist can initiate multiple second-messenger systems leading to similar changes in voltage-activated calcium current activity. The modulatory action on calcium currents produced by one second-messenger system added to the modulatory action resulting from activation of the other second-messenger system. The effect is to alter the magnitude of the horizontal cell calcium currents.

Animals↗
PubMed2001

Nerve growth factor is expressed by postmitotic avian retinal horizontal cells and supports their survival during development in an autocrine mode of action.

Cell death in the developing retina is regulated, but so far little is known about what factors regulate the cell death. Several neurotrophic factors and receptors, including the neurotrophins and Trk receptors, are expressed during the critical time. We have studied the developing avian retina with respect to the role of nerve growth factor (NGF) in these processes. Our starting point for the work was that NGF and its receptor TrkA are expressed in a partially overlapping pattern in the inner nuclear layer of the developing retina. Our results show that TrkA and NGF-expressing cells are postmitotic. The first NGF-expressing cells were found on the vitreal side of the central region of E5.5-E6 retina. This pattern changed and NGF-expressing cells identified as horizontal cells were later confined to the external inner nuclear layer. We show that these horizontal cells co-express TrkA and NGF, unlike a subpopulation of amacrine cells that only expresses TrkA. In contrast to the horizontal cells, which survive, the majority of the TrkA-expressing amacrine cells die during a period of cell death in the inner nuclear layer. Intraocular injections of NGF protein rescued the dying amacrine cells and injection of antisense oligonucleotides for NGF that block its synthesis, caused death among the TrkA-expressing horizontal cells, which normally would survive. Our results suggest that NGF supports the survival of TrkA expressing avian horizontal cells in an autocrine mode of action in the retina of E10-E12 chicks. The cells co-express TrkA and NGF and the role for NGF is to maintain the TrkA-expressing horizontal cells. The TrkA-expressing amacrine cells are not supported by NGF and subsequently die. In addition to the effect on survival, our results suggest that NGF plays a role in horizontal cell plasticity.

Animals↗
PubMed1995

Intracellular alkalinization enhances inward rectifier K+ current in retinal horizontal cells of catfish.

Isolated cone-driven horizontal cells dissociated from catfish retina were voltage-clamped using the whole-cell patch-clamp technique. The effects of acidification and alkalinization on an anomalous type, inwardly-rectifying K+ current (IRK+) were investigated. The magnitude of IRK+ was enhanced by raising the intracellular pH above 7.4, however, in contrast, intracellular acidification had little effect on this current. The range over which intracellular pH ([pH]i) modulates IRK+ is different from that for modulation of a sustained high-voltage activated calcium current in these same cells and also for proton-sensitive, inward rectifier currents in starfish oocytes, skeletal muscle and heart myocytes.

Animals↗
PubMed1975

[The non-synaptic membrane of the retinal horizontal cells as an amplifier of slow potentials].

A simplified model of the membrane of horizontal cells of L-type is suggested. The model reflects two main features of these cells studied earlier experimentally: 1) their hyperpolarizing response to light results from a decrease in EPSP maintained continuously in the dark; 2) the resistance of nonsynaptic membrane of these cells drops under hyperpolarization within a physiological range (from 0 to 70 mV). The model reproduces such properties of horizontal cells as a low membrane potential in the dark, inversion of the response to light with depolarization above a zero level of the membrane potential, an effect of mutual amplification of colour signals, saturation of the response in the bright light, peculiarities of stationary V-A-characteristics in the dark and in the light, as well as a shape of stationary relations between the membrane potential and light intensity which often have a steep part within a certain range of membrane potentials. The existence of hysteresis loops in V-A-characteristics and relations between the membrane potential and light intensity predicted by the model was confirmed experimentally in horizontal cells of fish retina. The analysis of the model and experimental results show that the nonsynaptic membrane of horizontal cells is able to amplify actively the slow graded potentials.

Animals↗