ArticleActa ophthalmologica2011
Two separate Ni(2+) -sensitive voltage-gated Ca(2+) channels modulate transretinal signalling in the isolated murine retina.
Article in Acta ophthalmologica, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed, 12 citations in OpenAlex.
- Retinal Vessel Responses to Flicker Stimulation Are Impaired in CaFrontiers in neurology · 2021Article
- Submicromolar copper (II) ions stimulate transretinal signaling in the isolated retina from wild type but not from CaBMC ophthalmology · 2020Article
- Unconjugated bilirubin modulates neuronal signaling only in wild-type mice, but not after ablation of the R-type/CaCNS neuroscience & therapeutics · 2018Article
- Evaluation of micro Electroretinograms Recorded with Multiple Electrode Array to Assess Focal Retinal Function.Scientific reports · 2016Article
- Low concentrations of ethanol but not of dimethyl sulfoxide (DMSO) impair reciprocal retinal signal transduction.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
purposeLight-evoked responses from vertebrate retinas were recorded as an electroretinogram (ERG). The b-wave is the most prominent component of the ERG, and in the bovine retina its NiCl(2) -sensitive component was attributed to reciprocal signalling by pharmacoresistant R-type voltage-gated Ca(2+) channels, which similar to other voltage-dependent Ca(2+) channels trigger and control neurotransmitter release. The murine retina has the great advantage that the effect of gene inactivation for Ni(2+) -sensitive Ca(2+) channels can be analysed to prove or disprove that any of these Ca(2+) channels is involved in retinal signalling.
methodsSuperfused retinas from different murine genotypes lacking either one or both highly Ni(2+) -sensitive voltage-gated Ca(2+) channels were used to record their ex vivo ERGs.
resultsThe isolated retinas from mice lacking Ca(v)2.3 R-type or Ca(v)3.2 T-type or both voltage-gated Ca(2+) channels were superfused with a NiCl(2) (15 μm) containing nutrient solution. The change in the b-wave amplitude and implicit time, caused by NiCl(2), was calculated as a difference spectrum and compared to data from control animals. From the results, it can be deduced that Ca(v)2.3 contributes rather to a later component in the b-wave response, while in the absence of Ca(v)3.2 the gain of Ni(2+) -mediated increase in the b-wave amplitude is significantly increased, probably due to a loss of reciprocal inhibition to photoreceptors. Thus, each of the Ni(2+)-sensitive Ca(2+) channels contributes to specific features of the b-wave response.
conclusionBoth high-affinity Ni(2+)-sensitive Ca(2+) channels contribute to transretinal signalling. Based on the results from the double knockout mice, additional targets for NiCl(2) must contribute to transretinal signalling, which will be most important for the structurally similar physiologically more important heavy metal cation Zn(2+).
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