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PubMed1997

The role of retinal bipolar cell in early vision: an implication with analogue networks and regularization theory.

A linear analogue network model is proposed to describe the neuronal circuit of the outer retina consisting of cones, horizontal cells, and bipolar cells. The model reflects previous physiological findings on the spatial response properties of these neurons to dim illumination and is expressed by physiological mechanisms, i.e., membrane conductances, gap-junctional conductances, and strengths of chemical synaptic interactions. Using the model, we characterized the spatial filtering properties of the bipolar cell receptive field with the standard regularization theory, in which the early vision problems are attributed to minimization of a cost function. The cost function accompanying the present characterization is derived from the linear analogue network model, and one can gain intuitive insights on how physiological mechanisms contribute to the spatial filtering properties of the bipolar cell receptive field. We also elucidated a quantitative relation between the Laplacian of Gaussian operator and the bipolar cell receptive field. From the computational point of view, the dopaminergic modulation of the gap-junctional conductance between horizontal cells is inferred to be a suitable neural adaptation mechanism for transition between photopic and mesopic vision.

Animals↗
PubMed1990

Hydroxyindole-O-methyltransferase in rat retinal bipolar cells: persistence following photoreceptor destruction.

The presence of hydroxyindole-O-methyltransferase (HIOMT) activity and localization of HIOMT immunoreactivity was examined in albino rat retinas following photoreceptor destruction. Male Sprague-Dawley rats were exposed to high intensity fluorescent light for 4 consecutive days, then placed on a 14:10 h light:dark cycle for two weeks to allow for phagocytic removal of damaged cells from the retina. Histologic examination revealed almost complete destruction and removal of all photoreceptors. The damaged retinas exhibited an increase in HIOMT activity relative to controls, when expressed as activity per mg of protein. HIOMT activity in the pineal glands was not affected. When control and light damaged retinas were examined for HIOMT localization by immunocytochemistry, the control retinas displayed intense HIOMT immunoreactivity in all photoreceptors, and a somewhat lighter labeling in a population of bipolar cells, whereas the light damaged retinas (lacking photoreceptors) showed intense HIOMT immunoreactivity in bipolar cells. These results suggest that the increase in HIOMT activity following photoreceptor destruction is due to increased synthesis of this enzyme in a population of bipolar cells. These HIOMT-immunoreactive bipolar cells may perhaps respond in a compensatory manner to changing levels of melatonin in the retina.

Acetylserotonin O-Methyltransferase↗
PubMed1990

Intracellular cesium separates two glutamate conductances in retinal bipolar cells of goldfish.

The responses of depolarizing bipolar cells to glutamate were investigated in the superfused isolated goldfish retina. In intracellular recordings with potassium-filled microelectrodes, glutamate hyperpolarized cells but did not alter the net input conductance. In recordings with cesium-filled microelectrodes, the glutamate-evoked hyperpolarization was associated with a net conductance decrease. In the presence of internal cesium, glutamate action had the same reversal potential as the actions of the glutamate analog 2-amino-4-phosphonobutyrate (APB) and the rod transmitter, suggesting that all three of these substances act at the same class of receptor. We propose that glutamate acts both at the APB-sensitive receptor that mediates rod inputs and at another receptor type that produces a conductance increase, is blocked by cesium, and may mimic the action of the cone transmitter.

Aminobutyrates↗
PubMed1995

Ca(2+)-dependent Cl- current at the presynaptic terminals of goldfish retinal bipolar cells.

In ON-type bipolar cells dissociated from the goldfish retina, a slowly declining inward current (Itail) was observed after the termination of depolarizing voltage step commands, during which a Ca2+ current was elicited. The properties of Itail were investigated under the whole-cell voltage clamp. Introduction of the membrane permeant Ca2+ chelator, BAPTA/AM, into the cell suppressed Itail, indicating that Itail was activated by the increase of intracellular free Ca2+ concentration ([Ca2+]i). The major component of Itail was identified as the Ca(2+)-dependent Cl- current (ICl(Ca)), since the reversal potential of Itail was almost identical to the Cl- equilibrium potential at various extracellular Cl- concentrations ([Cl-]o). The contribution of the Na+/Ca2+ exchanger current to Itail was very small. ICl(Ca) was partially suppressed by 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid (SITS) when it was locally applied to the axon terminal but not to the cell body region, suggesting that Ca(2+)-dependent Cl- channels were localized to the axon terminal. The relationship between the peak amplitude of ICl(Ca) and the amount of charge carried by the Ca2+ current was almost linear at levels less than ca. 50 pC, but became saturated at a higher Ca2+ charge.

Animals↗
PubMed1991

Membrane currents and pharmacology of retinal bipolar cells: a comparative study on goldfish and mouse.

We obtained solitary bipolar cells using enzymatic (papain) dissociation of the goldfish and mouse (C57BL/6J, adult) retinae and measured the membrane currents of these cells by whole-cell patch clamp. Bipolar cells of these two species showed two main differences. A. Ca current 1. In the mouse, depolarization evoked a transient Ca current that had maximal amplitude at about -30 mV. 2. The Ca conductance was activated by voltage steps to potentials greater than -60 mV and inactivated fully at potentials greater than -20 mV. 3. The mouse Ca current was insensitive to Cd2+ or dihydropyridine. 4. Contrary to mouse, goldfish bipolar cells had a sustained Ca current, which was activated over a more positive potential range (greater than -30 mV), blocked by either 50 microM Cd2+ or 10 microM nifedipine, and markedly augmented by 10 microM Bay K8644. 5. The transient character of the Ca current in mouse bipolar cells may help to shape phasic responses of ganglion cells, while in goldfish the sustained nature of Ca current may contribute to shape tonic responses of ganglion cells. B. Pharmacology 1. We examined the effects of the inhibitory transmitters, glycine and GABA, on bipolar cells. 2. GABA produced strong inhibitory effects on bipolar cells of both goldfish and mouse. 3. The highest GABA sensitivity was found at the bipolar cell axon terminal, the site of reciprocal connection with amacrine cells. 4. GABA increased the Cl conductance. 5. Unlike GABA, glycine was effective only on the mouse bipolar cells. Axon terminals showed the highest glycine sensitivity. 6. Glycine-induced currents were also carried by Cl ions. 7. Since ECl in intact cells is assumed to be -55 mV, both GABA and glycine are thought to generate hyperpolarizing responses in cells maintained at their resting potential (ca. -45 mV). 8. The present study suggests that inhibition from amacrine cells to bipolar cells, found in both species, is mediated by different transmitters.

Animals↗
PubMed1991

cGMP-gated conductance in retinal bipolar cells is suppressed by the photoreceptor transmitter.

Transmitter release from photoreceptors is decreased by light, resulting in a conductance increase in depolarizing bipolar cells. Addition of exogenous cGMP through a patch pipette to depolarizing bipolar cells from slices of dark-adapted tiger salamander retina resulted in an enhancement of the light response. This enhancement was blocked by GTP-gamma-S and dipyridamole, an inhibitor of phosphodiesterase. GTP-gamma-S and dipyridamole also blocked responses to exogenously applied 2-amino-4-phosphonobutyrate (APB), the glutamate agonist selective for this receptor. These data support the hypothesis that the postsynaptic receptor is linked via a G protein to a phosphodiesterase. The binding of glutamate or APB to the receptor suppresses a cGMP-activated current by increasing the rate of cyclic nucleotide hydrolysis.

Alkaloids↗
PubMed1999

Regulation of transmitter release from retinal bipolar cells.

Mb1 bipolar cells (ON-type cells) of the goldfish retina have exceptionally large (approximately 10 microns in diameter) presynaptic terminals, and thus, are suitable for investigating presynaptic mechanisms for transmitter release. Using enzymatically dissociated Mb1 bipolar cells under whole-cell voltage clamp, we measured the Ca2+ current (ICa), the intracellular free Ca2+ concentration ([Ca2+]i), and membrane capacitance changes associated with exocytosis and endocytosis. Release of transmitter (glutamate) was monitored electrophysiologically by a glutamate receptor-rich neuron as a probe. L-type Ca2+ channels were localized at the presynaptic terminals. The presynaptic [Ca2+]i was strongly regulated by cytoplasmic Ca2+ buffers, the Na(+)-Ca2+ exchanger and the Ca2+ pump in the plasma membrane. Once ICa was activated, a steep Ca2+ gradient was created around Ca2+ channels; [Ca2+]i increased to approximately 100 microM at the fusion sites of synaptic vesicles whereas up to approximately 1 microM at the cytoplasm. The short delay (approximately 1 ms) of exocytosis and the lack of prominent asynchronous release after the termination of ICa suggested a low-affinity Ca2+ fusion sensor for exocytosis. Depending on the rate of Ca2+ influx, glutamate was released in a rapid phasic mode as well as a tonic mode. Multiple pools of synaptic vesicles as well as vesicle cycling seemed to support continuous glutamate release. Activation of protein kinase C increased the size of synaptic vesicle pool, resulting in the potentiation of glutamate release. Goldfish Mb1 bipolar cells may still be an important model system for understanding the molecular mechanisms of transmitter release.

Animals↗
PubMed1997

Two components of transmitter release in retinal bipolar cells: exocytosis and mobilization of synaptic vesicles.

Ca2+-transmitter release coupling was examined using bipolar cells with large presynaptic terminals dissociated from the goldfish retina. Presynaptic Ca2+ current (I(Ca)) was recorded under the whole-cell voltage clamp. Release of excitatory amino acid transmitter was simultaneously monitored as the current through N-methyl-D-asperate (NMDA) receptors of reporter cells or as the membrane capacitance (C(m)) change associated with exocytosis. When I(Ca) was activated by a long depolarizing pulse, a double-peaked transmitter-induced current (I(tr)) was elicited in reporter cells. The rapid component of I(tr) was evoked immediately after the onset of depolarization, and was affected only slightly by intracellularly applied Ca2+ chelators. The delayed slow component of I(tr) was elicited during depolarization once a fixed amount of Ca2+ was accumulated in presynaptic terminals, and its appearance was suppressed or retarded by Ca2+ chelators. Two components of transmitter release were also recognized by monitoring C(m) changes elicited by the activation of I(Ca). These results suggest that bipolar cells have at least two pools of synaptic vesicles; a small, immediately releasable pool and a large releasable pool. The rapid and the delayed slow components of transmitter release may reflect exocytosis and mobilization of synaptic vesicles, respectively.

Animals↗
PubMed1999

Characterization of spontaneous excitatory synaptic currents in newt retinal bipolar cells.

The kinetics of glutamate concentration in the synaptic cleft is an important determinant of synaptic function. To elucidate peak concentration of glutamate released from a single vesicle in the cleft, spontaneous excitatory postsynaptic currents (sEPSCs) in Off-bipolar cells from the sliced newt retina were analyzed using whole-cell patch clamp recording and the computer simulation. The sEPSCs were blocked by an AMPA/kainate (KA) antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), and prolonged by cyclothiazide. However, an N-methyl-D-aspartate (NMDA) antagonist, D-2-amino-5-phosphonopentanoic acid (D-AP5), was ineffective. These suggest that sEPSCs in Off-bipolar cells are mediated exclusively by AMPA/KA receptors. sEPSCs simulated by a detailed kinetic model of AMPA receptor best approximated the data, when peak glutamate concentration was 10 microM. Therefore, it was concluded that peak concentration of glutamate released from a single vesicle would be elevated to approximately 10 microM at the newt Off-bipolar dendrite.

2-Amino-5-phosphonovalerate↗
PubMed2002

A membrane marker leaves synaptic vesicles in milliseconds after exocytosis in retinal bipolar cells.

Perhaps synaptic vesicles can recycle so rapidly because they avoid complete exocytosis, and release transmitter through a fusion pore that opens transiently. This view emerges from imaging whole terminals where the fluorescent lipid FM1-43 seems unable to leave vesicles during transmitter release. Here we imaged single, FM1-43-stained synaptic vesicles by evanescent field fluorescence microscopy, and tracked the escape of dye from single vesicles by watching the increase in fluorescence after exocytosis. Dye left rapidly and completely during most or all exocytic events. We conclude that vesicles at this terminal allow lipid exchange soon after exocytosis, and lose their dye even if they connected with the plasma membrane only briefly. At the level of single vesicles, therefore, observations with FM1-43 provide no evidence that exocytosis of synaptic vesicles is incomplete.

Animals↗
PubMed1988

Retinal bipolar cells receive negative feedback input from GABAergic amacrine cells.

Bipolar cells make reciprocal synapses with amacrine cells in the inner plexiform layer; both feedforward connections and feedback connections are present. The physiological properties of the feedback synapse have not been well described. Since some amacrine cells are thought to be GABAergic, we examined bipolar cells for feedback input from gamma-aminobtyric acid (GABA)ergic amacrine cells. Solitary bipolar cells were dissociated enzymatically from the goldfish retina. Cells were voltage clamped with a patch pipette and their GABA sensitivity was examined. GABA evoked responses in all bipolar cells with a large axon terminal, which were identified to be the rod dominant ON type, and in some bipolar cells with a small axon terminal. The highest GABA sensitivity was located at the axon terminal. The least effective dose was as low as 100 nM. A small insignificant response of high threshold was evoked when GABA was applied to the dendrite and soma. GABA increased the Cl conductance and caused membrane hyperpolarization. The bipolar cells had the GABAA receptor coupled with a benzodiazepine receptor. The GABA-evoked response was not susceptible to Co ions, which suppressed the GABA-induced responses in turtle cones by 50% at 5 microM concentration. Incomplete desensitization was observed, suggesting that the GABAergic pathway seems capable of transmitting signals tonically. The present results strongly indicate that the rod-dominant ON-type bipolar cells and some bipolar cells with a small axon terminal receive negative feedback inputs from GABAergic amacrine cells.

Action Potentials↗
PubMedDate not supplied

Retinal bipolar cells: contrast encoding for sinusoidal modulation and steps of luminance contrast.

Contrast encoding for sinusoidal modulations of luminance contrast was investigated by intracellular recording in the intact salamander retina. In what appears to be the first study of this kind for vertebrate bipolar cells, responses of the central receptive-field mechanism of cone-driven cells to modulation of 3 Hz were analyzed quantitatively via both signal averaging and a Fast Fourier Transform (FFT) while the retina was light adapted to 20 cd/m2. Depolarizing and hyperpolarizing bipolar cells showed very similar encoding. Both responded with sinusoidal waveforms whose amplitude varied linearly with modulation depths ranging up to 7-8%. The slope of the modulation/response curve was very steep in this range. Thus, the contrast gain was high, reaching values of 6-7, and the half-maximal response was achieved at modulations of 9% or less. At modulations above approximately 15%, the responses typically showed strong compressive nonlinearity and the waveform was increasingly distorted. At maximum modulation, the higher harmonics of the FFT constituted about 30% of the amplitude of the fundamental. Measurements were also made for cones and horizontal cells. Both cell types showed predominantly linear responses and low contrast gain, in marked contrast to bipolar cells. These results suggest that the high contrast gain and strong nonlinearity of bipolar cells largely arise postsynaptic to cone transmitter release. Further experiments were performed to compare responses to contrast steps versus those to sinusoidal modulation. In the linear range, we show that the contrast gains of cones and horizontal cells are low and virtually identical for both steps and sinusoidal modulations. In bipolar cells, on the other hand, the contrast gain is about two times greater for steps than that for the 3-Hz sine waves. These results suggest that mechanisms intrinsic to bipolar cells act like a high-pass filter with a short time constant to selectively emphasize contrast transients over slower changes in contrast.

Ambystoma↗
PubMedDate not supplied

The intrinsic dynamics of retinal bipolar cells isolated from tiger salamander.

We studied how intrinsic membrane properties affect the gain and temporal pattern of response in bipolar cells dissociated from retinae of tiger salamanders. Currents specified by a pseudorandom binary sequence, an m-sequence, superimposed on various means, were injected into the cells. From the resultant membrane voltage response for each mean current, impulse responses were estimated. From each impulse response, transfer function, gain, and time constant were calculated. The bipolar cells acted as quasilinear adaptive filters whose gain and response speed are determined by the mean input current. Near resting potential, gain. and time constant were maximum. Dynamics were slow and low-pass, characterized by an approximately exponential impulse response. With depolarization, gains were reduced sharply, responses were much faster, and dynamics became band-pass, as indicated by an undershoot in the impulse response. For any given mean current, the shape of the impulse response did not depend on the amplitude of the m-sequence currents. Thus, bipolar cells behaved in a quasilinear fashion. The adaptive behavior was eliminated by blocking a potassium current, which implicates the role of a voltage-gated potassium conductance. Computer simulations on a model neuron including a delayed-rectifier reconstructed the observed behavior, and provided insight into other, less readily observable, parameters. Thus, bipolar cells, even when isolated, possess mechanisms which regulate, with unsuspected elaborateness, the sensitivities and dynamics of their responsiveness. Implications for adaptation and neuronal processing are discussed.

Ambystoma↗
PubMed1980

Different postsynaptic events in two types of retinal bipolar cell.

The first synapse in the vertebrate visual system is made between the photoreceptors and the biopolar cells. Bioplar cells fall into two distinct classes according to whether the cell hyperpolarizes or depolarizes to small centred spots of light. Most evidence indicates that the light-induced hyperpolarization of the photoreceptprs suppresses transmitter release from the synaptic terminals, and it is probable that the differences between the two bipolar cell classes results from the different actions of the photoreceptor transmitter. In analysing the membrane potential fluctuations in both types of bipolar cell we find that the voltage noise spectra differ. It is to be expected that postsynaptic noise would be composed of the sum of noise generated in and transmitted from the cones and the noise arising from the statistical nature of synaptic transmission. We report here evidence for two such components in the voltage noise spectra recorded from each type of bipolar cell. The differences in the frequency distribution of the presumed transmitter-related components indicates that the transmitter generates events of longer duration in the depolarizing biopolar cells.

Animals↗
PubMed1990

Suppression by glutamate of cGMP-activated conductance in retinal bipolar cells.

Depolarizing bipolar cells (DBCs) of the retina are the only neurons in the vertebrate central nervous system known to be hyperpolarized by the neurotransmitter glutamate. Both glutamate and its analogue L-2-amino-4-phosphonobutyrate (APB) hyperpolarize DBCs by decreasing membrane conductance. Furthermore, glutamate responses in DBCs slowly decrease during whole-cell recording, suggesting that the response involves a second messenger system. Here we report that intracellular cyclic GMP or GTP activates a membrane conductance that is suppressed by APB, resulting in an enhanced APB response. In the presence of GTP-gamma-S, APB causes an irreversible suppression of the conductance. Inhibitors of G-protein activation or phosphodiesterase activity decrease the APB response. Thus, the DBC glutamate receptor seems to close ion channels by increasing the rate of cGMP hydrolysis by a G protein-mediated process that is strikingly similar to light transduction in photoreceptors.

1-Methyl-3-isobutylxanthine↗