Zinc Chelation Enhances the Sensitivity of the ERG b-Wave in Dark-Adapted Skate Retina

Redenti, Stephen; Chappell, Richard L.

doi:10.2307/1543258

Cited by 10 publications

(7 citation statements)

References 11 publications

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“…The present findings may have a direct bearing on the results of recent studies showing that 100 -500 M histidine significantly enhances the electroretinographic b-wave responses in the dark-adapted retinas of both skate and zebrafish (13,14,15). Glutamate release and, presumably, the co-release of zinc are maximal in darkness, and their rapid reduction by a light flash elicits a voltage response in second-order neurons that is proportional to the magnitude of the decrease in neurotransmitter.…”

supporting

confidence: 71%

Histidine Suppresses Zinc Modulation of Connexin Hemichannels

Chappell

Qian²,

Zakevicius³

et al. 2004

The Biological Bulletin

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Zinc has been shown to modulate hemichannel currents of connexins Cx35 and Cx38 in Xenopus oocytes (1).In both cases the effects were biphasic; i.e., low concentrations of zinc enhanced, whereas higher concentrations decreased, the magnitudes of the voltage-activated hemichannel currents. The present study was designed to determine the effects of zinc on hemichannels formed by Cx26, a connexin reportedly expressed on dendrites of carp horizontal cells and implicated in a mechanism for photoreceptor feedback (2,3,4). In addition, we examined whether histidine, a zinc chelator, would block the action of zinc on Cx26 hemichannel currents, or would exert a direct effect on those currents.Methods for oocyte preparation and recording of connexin hemichannel currents followed procedures described previously (5). Briefly, Stage V-VI oocytes were removed from gravid female Xenopus, enzymatically dissociated and defolliculated, and then used to express human Cx26 connexin in the presence of an antisense oligomer to the endogenous oocyte connexin (Cx38 Voltage-activated membrane currents were recorded with a two-electrode voltage clamp. The two protocols we used gave equivalent results: (1) with the cell clamped at 0 mV, 10-s voltage steps were imposed from Ϫ50 mV to ϩ50 mV in 10-mV increments, and (2) from the holding potential of 0 mV, currents were recorded in response to voltage ramps extending from Ϫ100 mV to ϩ60 mV at a rate of 0.04 mV/ms. Figure 1 compares a representative record from an oocyte expressing Cx26 with those obtained from an antisenseinjected cell and one that was not injected but expressed Cx38, its endogenous connexin. Note the efficacy with which the antisense oligo suppressed the current mediated by Cx38, and the significantly greater membrane currents of Cx26 in response to both depolarizing and hyperpolarizing voltages. Figure 2A shows current recordings from oocytes expressing human Cx26 in MB and after the addition of various concentrations of zinc. In MB, a voltage ramp from Ϫ100 mV to ϩ60 mV elicited large currents at all potentials positive and negative to the reversal potential (Ϫ10 mV), suggesting that the hemichannels are constitutively open (5). In the presence of low (1 M) concentrations of zinc, the magnitude of the currents through Cx26 hemichannels was substantially enhanced. Higher concentrations of zinc, however, decreased these currents in a dose-dependendant fashion such that 10 M zinc reduced the hemichannel currents to the level seen in control MB solution, and 100 M and 1 mM zinc further decreased the hemichannel currents. The bar graphs of Figure 2B, taken from the data in Figure 2A, illustrate the effects of zinc on Cx26 hemichannel currents recorded at ϩ40 mV. Both the enhancement and inhibition by zinc of the Cx26 hemichannel current showed little voltage dependence. As shown in Figure 2C, the ratio of the membrane currents measured in zinc to those recorded in MB were virtually unchanged across the range of membrane voltage tested (from Ϫ100 mV to ϩ60 mV) for both low conc...

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supporting

confidence: 71%

Histidine Suppresses Zinc Modulation of Connexin Hemichannels

Chappell

Qian²,

Zakevicius³

et al. 2004

The Biological Bulletin

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“…In dark adapted skate and zebrafish retinas, zinc chelation enhanced ERG b-wave amplitude when recorded in the presence of picrotoxin and in an eyecup preparation that, however, varies clearly from our recording conditions of the isolated and superfused retina. 40,41 Picrotoxin acts as a GABA-A receptor antagonist, which would occlude the signalling via E-/R-type Ca 2+ channels to GABA-A receptors. Therefore, the results from skate and zebrafish may point to additional targets different from Ca v 2.3, which influence the b-wave amplitude differently.…”

Section: S a Siapich Et Almentioning

confidence: 99%

Effect of ZnCl₂and Chelation of Zinc Ions by N,N-Diethyldithiocarbamate (DEDTC) on the ERG b-Wave Amplitude from the Isolated Superfused Vertebrate Retina

Siapich

Wrubel

Albanna

et al. 2010

Current Eye Research

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“…2+ is concentrated in photoreceptor terminals and is proposed to be co-released with glutamate in synaptic vesicles (Akagi et al, 2001;Wu et al, 1993). The Zn 2+ chelator, histidine, enhances the ERG b-wave in fish retina (Redenti and Chappell, 2003;Rosenstein and Chappell, 2003). Zn 2+ released from photoreceptors might act at a number of pre-and post-synaptic sites.…”

Section: Ionic Modulation Of Calcium Channels: Chloride-reducing the mentioning

confidence: 99%

Synaptic transmission at retinal ribbon synapses

Heidelberger

Thoreson

Witkovsky

2005

Progress in Retinal and Eye Research

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231

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The molecular organization of ribbon synapses in photoreceptors and ON bipolar cells is reviewed in relation to the process of neurotransmitter release. The interactions between ribbon synapseassociated proteins, synaptic vesicle fusion machinery and the voltage-gated calcium channels that gate transmitter release at ribbon synapses are discussed in relation to the process of synaptic vesicle exocytosis. We describe structural and mechanistic specializations that permit the ON bipolar cell to release transmitter at a much higher rate than the photoreceptor does, under in vivo conditions. We also consider the modulation of exocytosis at photoreceptor synapses, with an emphasis on the regulation of calcium channels.

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Zinc Chelation Enhances the Sensitivity of the ERG b-Wave in Dark-Adapted Skate Retina

Cited by 10 publications

References 11 publications

Histidine Suppresses Zinc Modulation of Connexin Hemichannels

Histidine Suppresses Zinc Modulation of Connexin Hemichannels

Effect of ZnCl₂and Chelation of Zinc Ions by N,N-Diethyldithiocarbamate (DEDTC) on the ERG b-Wave Amplitude from the Isolated Superfused Vertebrate Retina

Synaptic transmission at retinal ribbon synapses

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Zinc Chelation Enhances the Sensitivity of the ERG b-Wave in Dark-Adapted Skate Retina

Cited by 10 publications

References 11 publications

Histidine Suppresses Zinc Modulation of Connexin Hemichannels

Histidine Suppresses Zinc Modulation of Connexin Hemichannels

Effect of ZnCl2and Chelation of Zinc Ions by N,N-Diethyldithiocarbamate (DEDTC) on the ERG b-Wave Amplitude from the Isolated Superfused Vertebrate Retina

Synaptic transmission at retinal ribbon synapses

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Effect of ZnCl₂and Chelation of Zinc Ions by N,N-Diethyldithiocarbamate (DEDTC) on the ERG b-Wave Amplitude from the Isolated Superfused Vertebrate Retina