Evidence map›Paper›PMID 9006971›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997

Disruption of the metallothionein-III gene in mice: analysis of brain zinc, behavior, and neuron vulnerability to metals, aging, and seizures.

J C Erickson, G Hollopeter, S A Thomas, G J Froelick, R D Palmiter

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
15.4field-weighted citation impact, top 1% 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

54 citing papers in PubMed, 250 citations in OpenAlex.

  1. Metallothionein III Mediates CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
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  3. Review
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  5. Article
  6. Article
  7. Review
  8. Review
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  11. ZnExperimental neurology · 2020
    Article
  12. Article
  13. αFrontiers in pharmacology · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. ZnExperimental neurology · 2018
    Article
  19. Article
  20. Metallothionein in Brain Disorders.Oxidative medicine and cellular longevity · 2017
    Review
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 2 institutions in 1 country.

J C EricksonThe Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle, Washington 98195-7370, USA.
G Hollopeter
S A Thomas
G J Froelick
R D Palmiter
Howard Hughes Medical Institute · USUniversity of Washington · US

Funding

METALLOTHIONEIN FUNCTION AND CARCINOGENESISR01CA061268 · NCI · UNIVERSITY OF WASHINGTON · PI PALMITER, RICHARD D · 1994 to 1997
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REGULATION OF METALLOTHIONEIN GENE EXPRESSIONR01HD009172 · NICHD · UNIVERSITY OF WASHINGTON · PI PALMITER, RICHARD D · 1985 to 1987
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TRANSGENIC APPROACHES TO NERVOUS SYSTEM DEVELOPMENTR37HD009172 · NICHD · UNIVERSITY OF WASHINGTON · PI PALMITER, RICHARD D · 1988 to 1997
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NCI NIH HHS CA-61268NICHD NIH HHS HD-09172
6 · The paper itself

Abstract

Metallothionein-III (MT-III), a brain-specific member of the metallothionein family of metal-binding proteins, is abundant in glutamatergic neurons that release zinc from their synaptic terminals, such as hippocampal pyramidal neurons and dentate granule cells. MT-III may be an important regulator of zinc in the nervous system, and its absence has been implicated in the development of Alzheimer's disease. However, the roles of MT-III in brain physiology and pathophysiology have not been elucidated. Mice lacking MT-III because of targeted gene inactivation were generated to evaluate the neurobiological significance of MT-III. MT-III-deficient mice had decreased concentrations of zinc in several brain regions, including hippocampus, but the pool of histochemically reactive zinc was not disturbed. Mutant mice exhibited normal spatial learning in the Morris water maze and were not sensitive to systemic zinc or cadmium exposure. No neuropathology or behavioral deficits were detected in 2-year-old MT-III-deficient mice, but the age-related increase in glial fibrillary acidic protein expression was more pronounced in mutant brain. MT-III-deficient mice were more susceptible to seizures induced by kainic acid and subsequently exhibited greater neuron injury in the CA3 field of hippocampus. Conversely, transgenic mice containing elevated levels of MT-III were more resistant to CA3 neuron injury induced by seizures. These observations suggest a potential role for MT-III in zinc regulation during neural stimulation.

Indexed as

GenesAgingAnimalsBehavior, AnimalBrainCadmiumDisease SusceptibilityGlial Fibrillary Acidic ProteinLearningMemoryMetallothionein 3MetalsMiceMice, KnockoutNerve Tissue ProteinsNeuronsCadmiumGlial Fibrillary Acidic ProteinMetallothionein 3MetalsNerve Tissue ProteinsZinc

Identifiers

PMID9006971
PMCPMC6793742
OpenAlexW1581055808

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.