Evidence map›Paper›PMID 22049441›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Opposing roles of voltage-gated Ca2+ channels in neuronal control of regenerative patterning.

Dan Zhang, John D Chan, Taisaku Nogi, Jonathan S Marchant

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

38 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Praziquantel Pretreatment ReducesTropical medicine and infectious disease · 2025
    Article
  3. Article
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  5. Natural variation in the binding pocket of a parasitic flatworm TRPM channel resolves the basis for praziquantel sensitivity.Proceedings of the National Academy of Sciences of the United States of America · 2023
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  10. Review
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  13. Article
  14. CaCold Spring Harbor perspectives in biology · 2019
    Review
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  18. Review
  19. Utilizing the planarian voltage-gated ion channel transcriptome to resolve a role for a CaBiochimica et biophysica acta. Molecular cell research · 2017
    Article
  20. Article
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

4 authors at 2 institutions in 1 country.

Dan ZhangDepartment of Pharmacology, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA.
John D Chan
Taisaku Nogi
Jonathan S Marchant
University of Minnesota, Duluth · USUniversity of Minnesota Medical Center · US

Funding

Functional architecture of IP3-evoked local Ca2+ signalsR01GM088790 · NIGMS · UNIVERSITY OF MINNESOTA · PI MARCHANT, JONATHAN S, SLAMA, JAMES T · 2009 to 2025
$4.7M
NIGMS NIH HHS GM088790NIGMS NIH HHS R01 GM088790
6 · The paper itself

Abstract

There is intense interest in developing methods to regulate proliferation and differentiation of stem cells into neuronal fates for the purposes of regenerative medicine. One way to do this is through in vivo pharmacological engineering using small molecules. However, a key challenge is identification of relevant signaling pathways and therein druggable targets to manipulate stem cell behavior efficiently in vivo. Here, we use the planarian flatworm as a simple chemical-genetic screening model for nervous system regeneration to show that the isoquinoline drug praziquantel (PZQ) acts as a small molecule neurogenic to produce two-headed animals with integrated CNSs following regeneration. Characterization of the entire family of planarian voltage-operated Ca(2+) channel α subunits (Ca(v)α), followed by in vivo RNAi of specific Ca(v) subunits, revealed that PZQ subverted regeneration by activation of a specific voltage-gated Ca(2+) channel isoform (Ca(v)1A). PZQ-evoked Ca(2+) entry via Ca(v)1A served to inhibit neuronally derived Hedgehog signals, as evidenced by data showing that RNAi of Ca(v)1A prevented PZQ-evoked bipolarity, Ca(2+) entry, and decreases in wnt1 and wnt11-5 levels. Surprisingly, the action of PZQ was opposed by Ca(2+) influx through a closely related neuronal Ca(v) isoform (Ca(v)1B), establishing a novel interplay between specific Ca(v)1 channel isoforms, Ca(2+) entry, and neuronal Hedgehog signaling. These data map PZQ efficacy to specific neuronal Ca(v) complexes in vivo and underscore that both activators (Ca(v)1A) and inhibitors (Ca(v)1B) of Ca(2+) influx can act as small molecule neurogenics in vivo on account of the unique coupling of Ca(2+) channels to neuronally derived polarity cues.

Indexed as

AnimalsAnimals, Genetically ModifiedAnthelminticsBehavior, Animalbeta CateninCalciumCalcium Channels, L-TypeCytoskeletal ProteinsFeeding BehaviorNerve RegenerationNervous SystemNeuronsPlanariansPraziquantelRNA InterferenceSequence AlignmentAnthelminticsbeta CateninCalciumCalcium Channels, L-TypeCytoskeletal ProteinsPraziquantelWnt1 Protein

Identifiers

PMID22049441
PMCPMC3380623
OpenAlexW2143664654

What OpenQuestion holds

Textmetadata
LicenceTDM
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.