Evidence map›Paper›PMID 9592098›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998

G protein-mediated inhibition of neuronal migration requires calcium influx.

A M Horgan, P F Copenhaver

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.8field-weighted citation impact, top 35% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Manduca Contactin Regulates Amyloid Precursor Protein-Dependent Neuronal Migration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  6. Review
  7. Article
  8. Amyloid precursor proteins interact with the heterotrimeric G protein Go in the control of neuronal migration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  9. Article
  10. Article
  11. PDGF receptor-{beta} modulates metanephric mesenchyme chemotaxis induced by PDGF AA.American journal of physiology. Renal physiology · 2009
    Article
  12. Review
  13. Article
  14. How to innervate a simple gut: familiar themes and unique aspects in the formation of the insect enteric nervous system.Developmental dynamics : an official publication of the American Association of Anatomists · 2007
    Review
  15. Article
  16. 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

2 authors at 1 institution in 1 country.

A M HorganDepartment of Cell and Developmental Biology, Oregon Health Sciences University, Portland, Oregon 97201, USA.
P F Copenhaver
Oregon Health & Science University · US

Funding

DEVELOPMENTAL ROLE OF G PROTEINS IN NEURONAL MIGRATIONR01NS035369 · NINDS · OREGON HEALTH AND SCIENCE UNIVERSITY · PI COPENHAVER, PHILIP F · 1995 to 2002
$879k
NINDS NIH HHS NS-35369
6 · The paper itself

Abstract

Neuronal migration is an essential feature of the developing nervous system, but the intracellular signaling mechanisms that regulate this process are poorly understood. During the formation of the enteric nervous system (ENS) in the moth Manduca sexta, the migration of an identified set of neurons (the EP cells) is regulated in part by the heterotrimeric guanyl-nucleotide binding protein (G protein) Goalpha. Using an in vivo culture preparation for developing embryos that allows direct access to the ENS, we have shown that EP cell migration is similarly regulated by intracellular Ca2+; treatments that increased intracellular Ca2+ inhibited the migratory process, whereas buffering intracellular Ca2+ induced aberrant migration onto inappropriate pathways. Imaging the spontaneous changes in intracellular Ca2+ within individual EP cells showed that actively migrating neurons exhibited only small fluctuations in intracellular Ca2+. In contrast, neurons that had reached the end of migration displayed large, transient Ca2+ spikes. Similar Ca2+ spikes were induced in the EP cells by G protein stimulation, an effect that was reversed by removal of external Ca2+. Stimulation of Go in individual EP cells (by injection of either activated Goalpha subunits or mastoparan) also inhibited migration in a Ca2+-dependent manner. These results suggest that the regulation of neuronal migration by G proteins involves a Ca2+-dependent process requiring Ca2+ influx.

Indexed as

AnimalsCaffeineCalcimycinCalciumCell MovementChelating AgentsEgtazic AcidEmbryo, NonmammalianGTP-Binding ProteinsIonomycinIonophoresManducaNervous SystemNeuronsPhosphodiesterase Inhibitors1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acidCaffeineCalcimycinCalciumChelating AgentsEgtazic AcidGTP-Binding ProteinsIonomycinIonophoresPhosphodiesterase Inhibitors

Identifiers

PMID9592098
PMCPMC6792790
OpenAlexW1583977712

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.