Evidence map›Paper›PMID 23843509›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Calcium release-dependent actin flow in the leading process mediates axophilic migration.

B Ian Hutchins, Ulrike Klenke, Susan Wray

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Forces to Drive Neuronal Migration Steps.Frontiers in cell and developmental biology · 2020
    Review
  7. Nasal Placode Development, GnRH Neuronal Migration and Kallmann Syndrome.Frontiers in cell and developmental biology · 2019
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. CCDC141 Mutations in Idiopathic Hypogonadotropic Hypogonadism.The Journal of clinical endocrinology and metabolism · 2017
    Article
  13. Article
  14. Observational
  15. Article
  16. Article
  17. Article
  18. From migration to settlement: the pathways, migration modes and dynamics of neurons in the developing brain.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2016
    Review
  19. Review
  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

3 authors at 2 institutions in 1 country.

B Ian HutchinsCellular and Developmental Neurobiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-9525, USA.
Ulrike Klenke
Susan Wray
National Institute of Neurological Disorders and Stroke · USNational Institute of General Medical Sciences · US

Funding

Development And Regulation Of The Luteinizing Hormone Releasing Hormone SystemZIANS002824 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI WRAY, SUSAN · 2009 to 2025
$41.2M
The Luteinizing Hormone Releasing Hormone SystemZ01NS002824 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI WRAY, SUSAN · 1991 to 2008
$4.9M
Intramural NIH HHS Z01 NS002824Intramural NIH HHS ZIA NS002824NINDS NIH HHS NS002824-21
6 · The paper itself

Abstract

Proper assembly of neural circuits requires newly born neurons to migrate from their place of origin to their final location. Little is known about the mechanisms of axophilic neuronal migration, whereby neurons travel along axon pathways to navigate to their destinations. Gonadotropin-releasing hormone (GnRH)-expressing neurons migrate along olfactory axons from the nose into the forebrain during development, and were used as a model of axophilic migration. After migrating, GnRH neurons are located in the hypothalamus and are essential for puberty and maintenance of reproductive function. To gain a better understanding of the mechanisms underlying axophilic migration, we investigated in mice the regulation of movement from calcium signals to cytoskeletal dynamics. Live imaging revealed robust calcium activity during axophilic migration, and calcium release through IP3 receptors was found to stimulate migration. This occurred through a signaling pathway involving the calcium sensor calcium/calmodulin protein kinase kinase, AMP-activated kinase, and RhoA/ROCK. By imaging GnRH neurons expressing actin-GFP or Lifeact-RFP, calcium release was found to stimulate leading process actin flow away from the cell body. In contrast, actin contractions at the cell rear were unaffected by this calcium signaling pathway. These findings are the first to test the regulation of cytoskeletal dynamics in axophilic migration, and reveal mechanisms of movement that have broad implications for the migration of other CNS populations.

Indexed as

ActinsAnimalsAxonsCalciumCell MovementFemaleGonadotropin-Releasing HormoneMaleMiceOlfactory PathwaysActinsCalciumGonadotropin-Releasing Hormone

Identifiers

PMID23843509
PMCPMC3724331
OpenAlexW2000278582

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.