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PubMedDate not supplied

Retinal bipolar cell types differ in their inventory of ion channels.

Bipolar cells were recorded in rat retinal slices to study the distribution of hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels. Patch-clamp whole cell measurements were combined with intracellular filling and recorded cells were morphologically identified. HCN channel isoforms HCN1-4 are differentially expressed in bipolar cells. Each bipolar cell type has a characteristic inventory of HCN channels. The combination of HCN channel currents and other voltage-gated currents can be used as a kind of "finger print" to electrophysiologically identify and classify bipolar cell types. Using this approach of combined electrophysiological and morphological classification we could identify a new ON-cone bipolar cell type.

Animals↗

PubMed1999

Caffeine-sensitive Ca2+ stores in carp retinal bipolar cells.

High K+- or caffeine-induced Ca2+ signal was studied in freshly dissociated carp retinal ON-type bipolar cells using a confocal laser-scanning microscope. In response to 35 mM K+ exposure, a rise in [Ca2+]i appeared in both the terminal and soma, but was absent after removal of external Ca2+ or in the presence of 100 microM nifedipine. It is indicated that, for high K+-induced increase of [Ca2+]i, Ca2+ influx through voltage-gated L-type Ca2+ channels is essential and Ca2+ entry through reversed Na+/Ca2+ exchange may be negligible. Interestingly, caffeine-induced elevation of [Ca2+]i was restricted to the soma, and could be abolished by 50 microM ryanodine, suggesting that caffeine-sensitive Ca2+ stores gated by ryanodine receptors were present in the soma but not in the terminal of bipolar cells. After treatment with 50 microM ryanodine for 20 min, the peak of the Ca2+ transients evoked by 35 mM K+ in the soma decreased to 48.2+/-5.7% of the control. The results suggest that depolarization-evoked Ca2+ influx can cause Ca2+ release from caffeine-sensitive Ca2+ stores, and in turn amplify Ca2+ signal in the soma of retinal bipolar cells.

Animals↗

PubMed1991

Feedforward lateral inhibition in retinal bipolar cells: input-output relation of the horizontal cell-depolarizing bipolar cell synapse.

Lateral inhibition is the ubiquitous strategy used by visual neurons for spatial resolution throughout the animal kingdom. It has been a puzzle whether lateral inputs in retinal bipolar cells are mediated by the horizontal cell (HC)-cone feedback synapse, by the HC-bipolar cell feedforward synapse, or by both. By blocking the central inputs of the depolarizing bipolar cells (DBCs) with L-2-amino-4-phosphonobutyrate, we were able to eliminate the contribution of the feedback synapse and to demonstrate the postsynaptic light response in DBCs mediated by the HC-DBC feedforward synapse. The HC-DBC feedforward synapse contributes roughly one-third of the surround response whereas the HC-cone-DBC feedback synapse probably contributes the rest.

Ambystoma↗

PubMed1991

Permeation of calcium ions through non-NMDA glutamate channels in retinal bipolar cells.

The conduction of calcium ions through glutamate-gated channels is important in the induction of long-term potentiation and may trigger other cellular changes. In retinal bipolar cells, which lack the N-methyl-D-aspartate (NMDA) type of glutamate-gated channel, calcium permeability through non-NMDA channels was examined. Changes in extracellular calcium concentration unexpectedly affected the reversal potential for glutamate-induced currents in a manner consistent with these channels being highly permeable to calcium. External magnesium ions promote desensitization of these non-NMDA channels in a voltage-independent way. Thus, in addition to non-NMDA channels that conduct only sodium and potassium, there is a class that is also permeable to calcium.

Ambystoma↗

PubMed1995

Ca2+ regulation in the presynaptic terminals of goldfish retinal bipolar cells.

1. To investigate regulation of the intracellular free Ca2+ concentration ([Ca2+]i) in presynaptic terminals, the Ca2+ current (ICa) and [Ca2+]i in axon terminals were simultaneously monitored in acutely dissociated retinal bipolar cells under whole-cell voltage clamp. 2. The recovery phase of the Ca2+ transient, which was evoked by activation of ICa, became slower when the Na(+)-Ca2+ exchanger was suppressed by removing extracellular Na+. 3. Inhibition of the plasma membrane Ca2+ pump produced by raising extracellular pH to 8.4 increased the basal [Ca2+]i and caused incomplete recovery from the Ca2+ transient. These effects were not observed in orthovanadate-loaded bipolar cells. 4. The Ca2+ transient was not significantly affected by ryanodine, caffeine, thapsigargin, Ruthenium Red or FCCP. Internal Ca2+ stores may not participate in shaping the Ca2+ transient. 5. The ratio of the peak amplitude of the Ca2+ transient to the total amount of Ca2+ influx became smaller as the size of the Ca2+ influx increased. This action was not affected by blockage of Ca2+ transporters in the plasma membrane, or by reduction of the rate of Ca2+ influx. The peak amplitude of the Ca2+ transient seemed to be determined by Ca2+ buffering substances with a positive co-operativity.

Animals↗

PubMed1995

Potentiation of Ca2+ transients in the presynaptic terminals of goldfish retinal bipolar cells.

1. To study a possible contribution of intracellular Ca2+ stores to the presynaptic Ca2+ regulation, the Ca2+ current (ICa) and the intracellular free Ca2+ concentration ([Ca2+]i) were simultaneously monitored in isolated goldfish retinal bipolar cells using the whole-cell voltage clamp procedure and fura-2 fluorimetry. 2. The Ca2+ transient triggered by the activation of ICa was potentiated when [Ca2+]i was increased by applying either a prepulse or a small steady depolarization. The potentiation seemed to be partly due to the release of Ca2+ from intracellular Ca2+ stores. 3. The intracellular Ca2+ release was reversibly inhibited by caffeine but was not affected by ryanodine, suggesting that Ca2+ is released through intracellular Ca2+ channels which differ from ryanodine receptor channels. 4. These results suggest that the intracellular Ca2+ release may contribute to the facilitation of transmitter release.

Animals↗

PubMed2005

Clathrin-dependent and clathrin-independent retrieval of synaptic vesicles in retinal bipolar cells.

Synaptic vesicles can be retrieved rapidly or slowly, but the molecular basis of these kinetic differences has not been defined. We now show that substantially different sets of molecules mediate fast and slow endocytosis in the synaptic terminal of retinal bipolar cells. Capacitance measurements of membrane retrieval were made in terminals in which peptides and protein domains were introduced to disrupt known interactions of clathrin, the AP2 adaptor complex, and amphiphysin. All these manipulations caused a selective inhibition of the slow phase of membrane retrieval (time constant approximately 10 s), leaving the fast phase (approximately 1 s) intact. Slow endocytosis after strong stimulation was therefore dependent on the formation of clathrin-coated membrane. Fast endocytosis occurring after weaker stimuli retrieves vesicle membrane in a clathrin-independent manner. All compensatory endocytosis required GTP hydrolysis, but only a subset of released vesicles were primed for fast, clathrin-independent endocytosis.

Adaptor Protein Complex 2↗

PubMed2002

Endogenous calcium buffers regulate fast exocytosis in the synaptic terminal of retinal bipolar cells.

Calcium-triggered exocytosis at the synapse is suppressed by addition of calcium chelators, but the effects of endogenous Ca(2+) buffers have not been tested. We find that 80% of Ca(2+) binding sites in the synaptic terminal of retinal bipolar cells were associated with mobile molecules that suppressed activation of Ca(2+)-sensitive K(+) channels with an efficiency equivalent to approximately 1.2 mM BAPTA. Removing these buffers caused a 30-fold increase in the number of vesicles released by Ca(2+) tail currents lasting approximately 0.5 ms and a 2-fold increase in the rapidly releasable pool of vesicles (RRP). The effects of BAPTA and EGTA indicate that vesicles comprising the RRP were docked at variable distances from Ca(2+) channels. We propose that endogenous Ca(2+) buffers regulate the size of the RRP by suppressing the release of vesicles toward the periphery of the active zone.

Animals↗

PubMed2003

Bulk membrane retrieval in the synaptic terminal of retinal bipolar cells.

The mechanism of bulk membrane uptake at the synapse remains poorly defined, although exocytosis of synaptic vesicles is followed by compensatory membrane retrieval into both small vesicles and large cisternas or vacuoles. We investigated bulk retrieval in the presynaptic terminal of retinal bipolar cells. Fluorescence imaging of the membrane dye FM1-43 indicated that Ca2+-triggered exocytosis was followed by endocytosis into small vesicles and larger vacuoles that could be selectively labeled using large fluorescent dextrans. Disruption of actin filaments with cytochalasin D or latrunculin B inhibited the formation and transport of vacuoles, but exocytosis and endocytosis continued at normal rates. Bulk retrieval was linked to remodeling of the actin network, and both processes were inhibited by 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one, an inhibitor of phosphatidylinositol 3-kinase (PI 3-kinase). The regulation of F-actin dynamics by Ca2+ and PI 3-kinase therefore played an important role in compensatory endocytosis at this synapse, but this role was confined to bulk membrane uptake. Capacitance measurements demonstrated that fast endocytosis and refilling of the rapidly releasable pool of vesicles were not dependent on F-actin or PI 3-kinase activity. The basic properties of bulk membrane retrieval at this synapse were very similar to macropinocytosis described in non-neural cells. Bulk retrieval did not play an essential role in maintaining the vesicle cycle during maintained stimulation, but we suggest that it may play a role in the structural plasticity of this synaptic terminal.

Actin Cytoskeleton↗

PubMed2002

Glycinergic synaptic transmission to bullfrog retinal bipolar cells is input-specific.

Glycinergic inhibitory postsynaptic currents (IPSCs) focally elicited at the dendrites and axon terminals were recorded from bipolar cells in the bullfrog retinal slice, using the whole-cell clamp technique. IPSCs driven by input from interplexiform cells at bipolar cell dendrites (ipc-IPSCs) had a much slower decay time constant (25.2 +/- 7.8 ms) than IPSCs driven by input from amacrine cells at bipolar cell axon terminals (ac-IPSCs) (14.7 +/- 5.5 ms). Furthermore, peak-scaled non-stationary noise analysis revealed that the weighted mean single-channel conductance of the glycine receptors underlying bipolar cell dendritic ipc-IPSCs (20.8 +/- 6.6 pS) was significantly larger than that of those underlying bipolar cell axon terminal ac-IPSCs (12.9 +/- 2.9 pS). These results demonstrate that glycinergic synaptic transmission with different properties at bipolar cell dendrites and axon terminals differentially mediates intraretinal centrofugal signal transfer from the inner retina to the outer retina provided by interplexiform cells and lateral inhibition offered by amacrine cells in the inner retina.

Animals↗

PubMed1987

Neurotransmitter-induced currents in retinal bipolar cells of the axolotl, Ambystoma mexicanum.

1. Whole-cell patch clamping was used to study the membrane properties of isolated bipolar cells and the currents evoked in them by putative retinal neurotransmitters. 2. Isolated bipolar cells show an approximately ohmic response to voltage steps over most of the physiological response range, with an average input resistance of 1.3 G omega and resting potential of -35 mV. These values are underestimates because of the shunting effect of the seal between the patch electrode and the cell membrane. Depolarization beyond -30 mV produces rapid activation (10-100 ms) of an outward current (carried largely by potassium ions), which then inactivates slowly (0.5-2 s). 3. Of five candidates for the photoreceptor transmitter, four (aspartate, N-acetylhistidine, cadaverine, putrescine) had no effect on bipolar cells. The fifth substance, L-glutamate, opened ionic channels with a mean reversal potential of -12 mV in some cells (presumed hyperpolarizing bipolar cells), and closed channels with a mean reversal potential of -13 mV in other cells (presumed depolarizing bipolar cells). 4. The conductance increase induced by glutamate in presumed hyperpolarizing bipolar cells was associated with an increase in membrane current noise. Noise analysis suggested a single-channel conductance for the glutamate-gated channel of 5.4 pS. The power spectrum of the noise increase required the sum of two Lorentzian curves to fit it, suggesting that the channel can exist in three states. 5. The conductance decrease induced by glutamate in presumed depolarizing bipolar cells was associated with a decrease in membrane current noise that could be described as the sum of two Lorentzian spectra, and which suggested a single-channel conductance of 11 pS. The noise decrease implies that the channels closed by glutamate are not all open in the absence of the transmitter. 6. GABA (gamma-aminobutyric acid) and glycine, transmitters believed to mediate lateral inhibition in the retina, open chloride channels in isolated bipolar cells, and increase the membrane current noise. Noise analysis suggested that the channels gated by GABA and glycine have conductances of 4.4 and 7.5 pS respectively. The noise spectra required the sum of two Lorentzian curves to fit them. 7. By whole-cell patch clamping cells in retinal slices, the synaptic transmitter released by photoreceptors was shown to close channels with an extrapolated reversal potential around -3 mV in depolarizing bipolar cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1997

Ca2+ -activated K+ current at presynaptic terminals of goldfish retinal bipolar cells.

Properties of the Ca2+ -activated K+ current (I[K(Ca)]) were investigated in bipolar cells isolated from the goldfish retina. Pharmacological experiments and single channel current recordings demonstrated that I[K(Ca)] represented currents through BK channels, which were confined mostly to the presynaptic terminal. The ensemble noise analysis of I[K(Ca)], which was evoked following the activation of presynaptic Ca2+ current, revealed that the single channel conductance and open probability (P(o)) were approximately 50 pS ([K+]o = 2.6 mM, [K+]i = 140 mM) and 0.6 at 0 mV, respectively. To estimate [Ca2+]i at the cytosolic side of BK channels, activation of I[K(Ca)] was examined in Ca2+-loaded bipolar cells bathed in Co2+ solution. [Ca2+]i was monitored using furaptra fluorimetry. It was found that [Ca2+]i ranged between 10 and 20 microM when P(o) was 0.6. A high concentration of BAPTA ( > 20 mM) was required to suppress I[K(Ca)]. Under this condition, channel number was reduced without changing P(o). Therefore, it is likely that some BK channels are co-localized with Ca2+ channels in presynaptic terminals of retinal bipolar cells.

Animals↗

PubMedDate not supplied

Spontaneous regenerative activity in mammalian retinal bipolar cells: roles of multiple subtypes of voltage-dependent Ca2+ channels.

Patch-clamp recordings were used to investigate the properties of the regenerative activity in acutely isolated bipolar cells from the rat retina. Spontaneous, pacemaker-like membrane potential oscillations were observed in all rod bipolar cells and the majority of cone bipolar cells. The waveform of the regenerative potential was stereotypical but distinct among different bipolar cell groups, especially between rod and cone bipolar cells. The spontaneous activity was completely blocked by Co2+, suggesting that Ca2+ influx through voltage-dependent Ca2+ channels was required for initiating such activity. Ca2+-induced Ca2+ release, however, was not found to be involved. The spontaneous activity was also blocked by mibefradil, a T-type Ca2+ channel antagonist. In contrast, application of nimodipine, an L-type Ca2+ current antagonist, affected mainly the waveform of the regenerative potential. This study shows that mammalian retinal bipolar cells in isolation are also capable of generating Ca2+-dependent spontaneous regenerative potential. However, T-type Ca2+ channels appear to be essential for the initiation of the spontaneous activity in mammalian bipolar cells.

Animals↗

PubMed2000

Inhibition of calcium signaling in terminal and soma of carp retinal bipolar cells by GABA.

AIM: To investigate the effect of activation of gamma-aminobutyric acid (GABA) receptors on high K(+)-evoked Ca2+ signaling in the terminal and soma of carp retinal ON-type bipolar cells. METHODS: Freshly dissociated carp retinal cells were loaded with fluo-3AM and then the fluorescence measurements were performed on a confocal laser-scanning microscope. RESULTS: Ca2+ signaling evoked by high K+ 35 mmol/L was completely suppressed in both the terminal and soma of bipolar cells by GABA 100 mumol/L. However, different results were found in the terminal and soma when only one subtype of GABA receptors was activated. While activation of either GABAA or GABAC receptors totally suppressed Ca2+ signaling in the soma, a gradual elevation of [Ca2+]i appeared in the terminal. GABA 10 mumol/L could also completely suppress Ca2+ signaling in the soma, but could only partially reduce Ca2+ signaling in the terminal. CONCLUSION: Activation of both GABAA and GABAC receptors could completely inhibit high K(+)-evoked Ca2+ signaling in the terminal and soma of carp retinal ON-type bipolar cells. While activation of either GABAA or GABAC receptors alone still totally suppressed Ca2+ signaling in the soma, a gradual elevation of [Ca2+]i appeared in the terminal, which may be due to desensitization of GABA receptors.

Animals↗

PubMedDate not supplied

Dopamine depletion with 6-OHDA enhances dopamine D1-receptor modulation of potassium currents in retinal bipolar cells.

Ascorbate modulates IK(V) of ON-type mixed rod/cone bipolar cells (Mb) in the goldfish retinal slice through a dopamine D1/G-protein/PKA-coupled mechanism. We investigated the effects of dopamine depletion with intraocular injections of 6-OHDA on IK(V) and its modulation by ascorbate over 1-7 weeks following 6-OHDA treatment. Dopamine depletion was verified by tyrosine hydroxylase immunocytochemistry. Slices were perfused in a saline containing 200 microM sodium ascorbate. One-second puffs of ascorbate-free saline (zero [AA]o), delivered through a 2-3 microm diameter pipette, were directed at the bipolar cells. IK(V) was recorded by conventional whole-cell patch-clamp methods. In normal retinas, puffs of zero [AA]o caused a rapid (<100 ms) suppression of IK(V) of about 50% that lasted for several minutes. This effect was blocked by 1 microM SCH23390 and was unaffected by 2 mM Co2+ or 5 microM spiperone. 6-OHDA treatment resulted in major effects. First, IK(V) was reduced by approximately 50% for weeks 1-6, recovering to a 20% reduction by week 7. Second, puffs of zero [AA]o enhanced IK(V) rather than suppressed it. The enhancement was blocked by SCH23390 and the PKA inhibitor, Wiptide, but was insensitive to spiperone. Third, all parts of the Mb bipolar cell (except for the axon) were sensitive to puffs of zero [AA]o in both normal and 6-OHDA-treated retinas. Fourth, bath application of 20 microM dopamine restored the amplitude of IK(V) but did not reverse the effects of puffed zero [AA]o. IK(V) was fit by two exponentials; all of the effects on IK(V) were on the amplitude of the components and not on the time constants. Chronic dopamine depletion caused reversible changes in the properties of K+ channels underlying IK(V), as well as a long-term change in the intracellular coupling mechanisms between D1-receptor activation and the modulation of IK(V).

Adrenergic Agents↗

PubMed2005

Retinal bipolar cell input mechanisms in giant danio. III. ON-OFF bipolar cells and their color-opponent mechanisms.

Whole cell patch recording was performed from morphologically identified cone-driven on-off bipolar cells (Cabs) in giant danio retinal slices to study their glutamate receptors and light-evoked responses. Specific agonists were puffed in the presence of cobalt, picrotoxin, and strychnine to identify glutamate receptors on these cells. Most Cabs responded to both the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate receptor agonist kainate and the excitatory amino acid transporter (EAAT) substrate D-aspartate, and both responses were localized to the dendrites. Kainate generated depolarizations whereas D-aspartate had E(rev) close to E(Cl) and generated hyperpolarizations, indicating that the AMPA/kainate receptors are sign-preserving, whereas the EAATs are sign-inverting. In response to white light, some Cabs gave on bipolar cell-like responses whereas others gave off bipolar cell-like ones, but many cells' responses had both on and off bipolar cell components. In response to appropriately colored center-selective stimuli, many Cabs responded to short and long wavelengths with opposite polarities and were thus double color-opponent. The depolarizing components of the responses to white or colored stimuli were suppressed by the EAAT blocker DL-threo-beta-benzyloxyaspartate (TBOA), whereas the hyperpolarizing components were reduced by the AMPA/kainate receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX). These results are consistent with the hypothesis that both EAATs and AMPA/kainate receptors are involved in the generation of light-evoked responses in Cabs and that they confer these cells with on and off bipolar cell properties, respectively. Cabs can generate double color-opponent center responses by receiving inputs from certain cones through EAATs and from other cones through AMPA/kainate receptors.

Animals↗

PubMed2002

Regulation of the retinal bipolar cell mGluR6 pathway by calcineurin.

Glutamate produces a hyperpolarizing postsynaptic potential in ON bipolar cells by binding to the metabotropic receptor mGluR6 and subsequently closing a cation-selective channel. It has been proposed that Ca(2+) influx through the cation channel triggers a depression of the synaptic potential. Here we report that this Ca(2+)-mediated depression requires activation of calcineurin, a Ca(2+)/calmodulin-regulated phosphatase. We measured glutamate-evoked currents (I(glu)) with whole cell recordings of ON bipolar cells in light-adapted retinal slices. Depression of I(glu) by Ca(2+) was prevented by inhibitors of calcineurin or by tightly buffering Ca(2+) with bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA). However, when cells were dialyzed with BAPTA and a Ca(2+)-independent form of calcineurin (CaN420), depression of I(glu) was restored. Similarly, CaN420 induced depression of I(glu) during continuous glutamate application, a protocol that ordinarily prevents depression. Analysis of changes in the amplitude of the cation-selective current (I(cat)) of cells that were dialyzed with high Ca(2+) (1 microM), or with BAPTA and CaN420, indicates that Ca(2+) depresses I(glu) by reducing I(cat) and that calcineurin acts via the same mechanism. Ca(2+)-mediated depression of I(glu) was not found to involve CaMKII, as inhibitors of CaMKII did not prevent this depression nor did they affect the sensitivity of the response to small changes in the concentration of mGluR6 agonist. Our data suggest that Ca(2+) and calcineurin may play an adaptive role at the synapse between photoreceptor and ON bipolar cells, closing postsynaptic cation channels that are opened by a drop in synaptic glutamate levels during prolonged photoreceptor illumination.

Animals↗

PubMed1997

Differential reinnervation of retinal bipolar cell dendrites and axon terminals by dopamine interplexiform cells following dopamine depletion with 6-OHDA.

Depletion of retinal dopamine in goldfish increases light sensitivity at photopic backgrounds. As horizontal cells appear not to be involved with this effect (Yazulla and Studholme [1995] Vis. Neurosci. 12:827-837), we investigated the innervation patterns of the ON rod/cone bipolar cells (ON-BC) by dopaminergic interplexiform cells (DA-IPCs) normally and during the period of neogeneration of new DA-IPCs at the marginal zone following DA-IPC destruction. DA-IPCs were destroyed via intraocular injection of 6-hydroxydopamine over 2 successive days. Controls and 1 year post-injection retinas were double labeled for protein kinase C and tyrosine hydroxylase (TH) immunocytochemistry to identify the ON-BCs and the DA-IPCs, respectively. Double-labeled 25 microns tissue sections were examined on a confocal laser scanning microscope by using dual channel immunofluorescence acquisition. Image stacks were analyzed for DA-IPC/ON-BC contacts in the distal inner nuclear layer (INL) and inner plexiform layer (IPL). Image stacks were rotated 180 degrees with respect to each other and reanalyzed to determine potential randomness of the contacts. For control retinas there were 1.8 contacts/axon terminal in the IPL (n = 165) and 9.4 contacts/ON-BC in the distal INL (n = 28). At 1 year after injection, reinnervation of TH-immunoreactive boutons in the retina recovered to 16% of control in the IPL but only 10% in the distal INL. Establishment of DA-IPC/ON-BC contacts recovered to 36% of control for ON-BC axon terminals (n = 103), whereas there was no recovery of contacts in the distal INL (n = 30). Reinnervation of ON-BC by DA-IPCs preferentially targets the axon terminals. The absence of reinnervation of bipolar cell dendrites by DA-IPCs may account for the persistence of the increased light sensitivity following retinal dopamine depletion. Thus, dopamine input to ON-BCs in the outer retina maybe involved in setting background sensitivity under photopic conditions.

Animals↗