ArticleExperimental eye research2008
Zinc-mediated feedback at the synaptic terminals of vertebrate photoreceptors.
Article in Experimental eye research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Ultrastructural Characteristics and Synaptic Connectivity of Photoreceptors in the Simplex Retina of Little Skate (eNeuro · 2023Article
- Submicromolar copper (II) ions stimulate transretinal signaling in the isolated retina from wild type but not from CaBMC ophthalmology · 2020Article
- Voltage- and calcium-gated ion channels of neurons in the vertebrate retina.Progress in retinal and eye research · 2019Review
- Zinc in Wound Healing Modulation.Nutrients · 2017Review
- Cytoprotection by endogenous zinc in the vertebrate retina.Journal of neurochemistry · 2014Article
- Zinc modulation of calcium activity at the photoreceptor terminal: a calcium imaging study.Experimental eye research · 2013Article
- Synaptic Zn2+ inhibits neurotransmitter release by promoting endocannabinoid synthesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- A reduced zinc diet or zinc transporter 3 knockout attenuate light induced zinc accumulation and retinal degeneration.Experimental eye research · 2013Article
- Regulation of synaptic transmission at the photoreceptor terminal: a novel role for the cation-chloride co-transporter NKCC1.The Journal of physiology · 2013Article
- Light-induced photoreceptor and RPE degeneration involve zinc toxicity and are attenuated by pyruvate, nicotinamide, or cyclic light.Molecular vision · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
There is mounting evidence that zinc release from glutamatergic nerve terminals serves as a neuromodulator at synaptic sites within the retina and CNS. However, it has not been possible to reliably measure the concentration of zinc co-released with glutamate in the confines of the synaptic cleft. Thus, much of the evidence supporting this view derives from electrophysiological studies showing the modulatory effects of exogenous zinc on the membrane currents of ligand- and voltage-gated channels. In the present study, we took advantage of the unique properties of the glutamatergic photoreceptor terminal to demonstrate a feedback signal mediated by endogenous zinc at the synaptic sites from which it is discharged. Through its ability to block voltage-gated calcium channels in the photoreceptor terminal, zinc suppresses the radial dark current of the visual cell, and reduces its release of glutamate. It follows that chelation of extracellular zinc, e.g., with histidine, will lead to an increase both in the dark current and in the release of glutamate, changes that result in an enhancement of the light-evoked a-wave of the ERG and can account for the b-wave enhancement observed previously after zinc chelation when inner retinal responses were not blocked by aspartate.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.