Evidence map›Paper›PMID 15900408›Full record

ArticleJournal of molecular histology2005

Endogenous zinc can be a modulator of glycinergic signaling pathway in the rat retina.

Makoto Kaneda, Katsuyoshi Ishii, Takumi Akagi, Tetsuya Tatsukawa, Tsutomu Hashikawa

Abstract read
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In one paragraph

Article in Journal of molecular histology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 28% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Zinc in eye health, retinal biology and disease.Progress in retinal and eye research · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Makoto KanedaDepartment of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan. mkaneda@sc.itc.keio.ac.jp
Katsuyoshi Ishii
Takumi Akagi
Tetsuya Tatsukawa
Tsutomu Hashikawa
RIKEN Center for Brain Science · JPKeio University · JPTokyo University of Pharmacy and Life Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zinc is a modulator of glutamatergic inputs in the hippocampus. In the retina, however, we previously reported that endogenous zinc is present in the non-glutamatergic neural processes and earlier electrophysiological studies suggest that zinc is a modulator of inhibitory signaling pathways, which are mediated by glycine and GABA. AII amacrine cells, a subpopulation of glycinergic amacrine cells, are identified by selective immunoreactivity for parvalbumin in the rat retina. In the present study, therefore, we focused on whether zinc is present in AII amacrine cells using silver amplification combined with immunohistochemistry in the rat retina. We also examined whether zinc modulate glycine response in the rat retina by the patch clamp technique. Association of silver precipitates with the parvalbumin-immunoreactive neural processes was observed at the ultrastructural level. We also found that zinc existed in the neural processes which were not parvalbumin-immunoreactive. Glycine-induced responses were augmented when the concentration of Zn(2+) was below 10 microM, but inhibited at Zn(2+) concentrations of 50 microM or more. Our results suggest the notion that zinc in neural processes of retinal neurons modulates the inhibitory signaling pathway, particularly that mediated by glycine receptors in AII amacrine cells.

Indexed as

AnimalsCell PolarityGlycineImmunohistochemistryMicroscopy, ConfocalMicroscopy, FluorescenceMicroscopy, ImmunoelectronNeuronsParvalbuminsPatch-Clamp TechniquesPhotoreceptor Cells, VertebrateRatsRats, WistarRetinaSignal TransductionZincGlycineParvalbuminsZinc

Identifiers

PMID15900408
OpenAlexW2054134808

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.