Evidence map›Paper›PMID 12952919›Full record

ArticleThe Journal of clinical investigation2003

Alimentary tract innervation deficits and dysfunction in mice lacking GDNF family receptor alpha2.

Jari Rossi, Karl-Heinz Herzig, Vootele Võikar, Païvi H Hiltunen, Mikael Segerstråle, Matti S Airaksinen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
  2. Time-resolved morphological and transcriptomic characterization of early enteric neuron subtype emergence in chick.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. scRNA-Seq Reveals New Enteric Nervous System Roles for GDNF, NRTN, and TBX3.Cellular and molecular gastroenterology and hepatology · 2021
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. The developmental etiology and pathogenesis of Hirschsprung disease.Translational research : the journal of laboratory and clinical medicine · 2013
    Review
  17. Article
  18. Article
  19. Article
  20. Cannabinoid receptor 1 in the vagus nerve is dispensable for body weight homeostasis but required for normal gastrointestinal motility.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    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

6 authors at 2 institutions in 2 countries.

Jari RossiProgram in Molecular Neurobiology, Institute of Biotechnology, University of Helsinki, Helsinki, Finland.
Karl-Heinz Herzig
Vootele Võikar
Païvi H Hiltunen
Mikael Segerstråle
Matti S Airaksinen
University of Helsinki · FIUniversity of Eastern Finland · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Subsets of parasympathetic and enteric neurons require neurturin signaling via glial cell line-derived neurotrophic factor family receptor alpha2 (GFRalpha2) for development and target innervation. Why GFRalpha2-deficient (Gfra2-/-) mice grow poorly has remained unclear. Here, we analyzed several factors that could contribute to the growth retardation. Neurturin mRNA was localized in the gut circular muscle. GFRalpha2 protein was expressed in most substance P-containing myenteric neurons, in most intrapancreatic neurons, and in surrounding glial cells. In the Gfra2-/- mice, density of substance P-containing myenteric ganglion cells and nerve bundles in the myenteric ganglion cell layer was significantly reduced, and transit of test material through small intestine was 25% slower compared to wild-type mice. Importantly, the knockout mice had approximately 80% fewer intrapancreatic neurons, severely impaired cholinergic innervation of the exocrine but not the endocrine pancreas, and increased fecal fat content. Vagally mediated stimulation of pancreatic secretion by 2-deoxy-glucose in vivo was virtually abolished. Retarded growth of the Gfra2-/- mice was accompanied by reduced fat mass and elevated basal metabolic rate. Moreover, the knockout mice drank more water than wild-type controls, and wet-mash feeding resulted in partial growth rescue. Taken together, the results suggest that the growth retardation in mice lacking GFRalpha2 is largely due to impaired salivary and pancreatic secretion and intestinal dysmotility.

Indexed as

Gastrointestinal MotilityAnimalsFemaleGlial Cell Line-Derived Neurotrophic Factor ReceptorsGrowth DisordersIntestinesMiceMice, Inbred C57BLNerve Growth FactorsNeurturinNutrition DisordersPancreasProto-Oncogene ProteinsProto-Oncogene Proteins c-retReceptor Protein-Tyrosine KinasesRNA, MessengerGfra2 protein, mouseGlial Cell Line-Derived Neurotrophic Factor ReceptorsNerve Growth FactorsNeurturinNrtn protein, mouseProto-Oncogene ProteinsProto-Oncogene Proteins c-retReceptor Protein-Tyrosine KinasesRNA, MessengerSubstance P

Identifiers

PMID12952919
PMCPMC182204
OpenAlexW2036137707

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.