Evidence map›Paper›PMID 17409232›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007

Prenatal exposure to elevated NT3 disrupts synaptic selectivity in the spinal cord.

Zhi Wang, Ling Ying Li, Michael D Taylor, Douglas E Wright, Eric Frank

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. 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
1.0field-weighted citation impact, top 28% 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, 30 citations in OpenAlex.

  1. Influencers in the Somatosensory System: Extrinsic Control of Sensory Neuron Phenotypes.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2023
    Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Synapse Formation in Monosynaptic Sensory-Motor Connections Is Regulated by Presynaptic Rho GTPase Cdc42.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  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

5 authors at 2 institutions in 1 country.

Zhi WangDepartment of Physiology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
Ling Ying Li
Michael D Taylor
Douglas E Wright
Eric Frank
Tufts University · USUniversity of Kansas Medical Center · 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 NS024373
6 · The paper itself

Abstract

Monosynaptic connections between muscle spindle (Ia) afferents and motoneurons (MNs), the central portion of the stretch reflex circuit, are highly specific, but the mechanisms underlying this specificity are primarily unknown. In this study, we report that embryonic overexpression of neurotrophin-3 (NT3) in muscles disrupts the development of these specific Ia-MN connections, using transgenic (mlc/NT3) mice that express elevated levels of NT3 in muscles during development. In mlc/NT3 mice, there is a substantial increase in the amplitudes of monosynaptic EPSPs evoked by Ia afferents in MNs as measured with extracellular recordings from ventral roots. Despite this increased functional projection of Ia afferents, there is no obvious change in the anatomical density of Ia projections into the ventral horn of the spinal cord. Intracellular recordings from MNs revealed a major disruption in the pattern of Ia-MN connections. In addition to the normal connections between Ia afferents and MNs supplying the same muscle, there were also strong monosynaptic inputs from Ia afferents supplying unrelated muscles, which explains the increase seen in extracellular recordings. There was also a large variability in the strength of Ia input to individual MNs, both from correct and incorrect Ia afferents. Postnatal muscular administration of NT3 did not cause these changes in connectivity. These results indicate that prenatal exposure to elevated levels of NT3 disrupts the normal mechanisms responsible for synaptic selectivity in the stretch reflex circuit.

Indexed as

Prenatal Exposure Delayed EffectsAnimalsFemaleMiceMice, Inbred C57BLMice, TransgenicNeurotrophin 3PregnancySpinal CordSynapsesSynaptic TransmissionNeurotrophin 3

Identifiers

PMID17409232
PMCPMC2562665
OpenAlexW2088320353

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.