Evidence map›Paper›PMID 18463181›Full record

ArticleJournal of neurophysiology2008

Early postnatal development of reciprocal Ia inhibition in the murine spinal cord.

Zhi Wang, LingYing Li, Martyn Goulding, Eric Frank

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
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  9. Review
  10. Review
  11. Article
  12. Contribution of the potassium-chloride cotransporter KCC2 to the strength of inhibition in the neonatal rodent spinal cord in vitro.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  13. Review
  14. Characterization of long descending premotor propriospinal neurons in the spinal cord.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  15. Inhibition downunder: an update from the spinal cord.Current opinion in neurobiology · 2014
    Review
  16. Article
  17. Article
  18. Article
  19. 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 1 institution in 1 country.

Zhi WangDepartment of Physiology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA. eric.frank@tufts.edu
LingYing Li
Martyn Goulding
Eric Frank
Tufts University · US

Funding

DEVELOPMENT OF SENSORY/MOTOR SYNAPSES IN THE SPINAL CORDR01NS024373 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FRANK, ERIC · 1986 to 2005
$2.6M
NINDS NIH HHS R01 NS024373NINDS NIH HHS R01 NS-24373
6 · The paper itself

Abstract

The pathway mediating reciprocal inhibition from muscle spindle afferents (Ia axons) to motoneurons (MNs) supplying antagonist muscles has been well studied in adult cats, but little is known about how this disynaptic pathway develops. As a basis for studying its development, we characterized this pathway in mice during the first postnatal week, focusing on the projection of quadriceps (Q) Ia axons to posterior biceps-semitendinosis (PBSt) MNs via Ia inhibitory interneurons. Synaptic potentials in PBSt MNs evoked by Q nerve stimulation are mediated disynaptically and are blocked by strychnine, implying that glycine is the major inhibitory transmitter as in adult cats. The specificity of neuronal connections in this reflex pathway is already high at birth; Q afferents evoke inhibitory synaptic potentials in PBSt MNs, but afferents supplying the adductor muscle do not. Similar to this disynaptic pathway in cats, Renshaw cells inhibit the interposed Ia interneurons, as they reduce the disynaptic input from Q axons but do not inhibit PBSt MNs directly. Reciprocal inhibition functionally inhibits the monosynaptic excitatory reflex in PBSt MNs by P3, but this functional inhibition is weak at P1. Finally, deletion of the transcription factor Pax6, which is required for the development of V1-derived Renshaw cells, does not block development of this pathway. This suggests either that Pax6 is not required for the phenotypic development of all V1-derived spinal interneurons or that these inhibitory interneurons are not derived from V1 precursors.

Indexed as

Reflex, MonosynapticAge FactorsAnimalsAnimals, NewbornBicucullineDose-Response Relationship, RadiationEye ProteinsGABA AntagonistsGlycine AgentsHomeodomain ProteinsInterneuronsIn Vitro TechniquesMiceMice, Inbred C57BLMice, KnockoutMotor NeuronsBicucullineEye ProteinsGABA AntagonistsGlycine AgentsHomeodomain ProteinsPaired Box Transcription FactorsPax6 protein, mousePAX6 Transcription FactorRepressor ProteinsStrychnine

Identifiers

PMID18463181
PMCPMC2493495
OpenAlexW2099450092

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.