Evidence map›Paper›PMID 20592209›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Synaptic scaling and the development of a motor network.

Laura D Knogler, Meijiang Liao, Pierre Drapeau

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Mechanisms underlying homeostatic plasticity in theProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  4. Article
  5. Article
  6. Article
  7. Spontaneous Release Regulates Synaptic Scaling in the Embryonic Spinal Network In Vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  8. Article
  9. A hybrid electrical/chemical circuit in the spinal cord generates a transient embryonic motor behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  10. Review
  11. Article
  12. Review
  13. Manipulations of spinal cord excitability evoke developmentally-dependent compensatory changes in the lamprey spinal cord.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2012
    Article
  14. 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 1 institution in 1 country.

Laura D KnoglerDepartment of Pathology and Cell Biology and Le Groupe de Recherche sur le Système Nerveux Central, Université de Montréal, Montréal, Québec H3T 1J4, Canada.
Meijiang Liao
Pierre Drapeau
Pharmacology Research Institute · US

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Neurons respond homeostatically to chronic changes in network activity with compensatory changes such as a uniform alteration in the size of miniature postsynaptic current (mPSC) amplitudes termed synaptic scaling. However, little is known about the impact of synaptic scaling on the function of neural networks in vivo. We used the embryonic zebrafish to address the effect of synaptic scaling on the neural network underlying locomotion. Activity was decreased during development by TTX injection to block action potentials or CNQX injection to block glutamatergic transmission. Alternatively TNFalpha was chronically applied. Recordings from spinal neurons showed that glutamatergic mPSCs scaled up approximately 25% after activity reduction and fortuitously scaled down approximately 20% after TNFalpha treatment, and were unchanged following blockade of neuromuscular activity alone with alpha-bungarotoxin. Regardless of the direction of scaling, immediately following reversal of treatment no chronic effect was distinguishable in motoneuron activity patterns or in swimming behavior. We also acutely induced a similar increase of glutamatergic mPSC amplitudes using cyclothiazide to reduce AMPA receptor desensitization or decrease of glutamatergic mPSC amplitudes using a low concentration of CNQX to partially block AMPA receptors. Though the strength of the motor output was altered, neither chronic nor acute treatments disrupted the patterning of synaptic activity or swimming. Our results show, for the first time, that scaling of glutamatergic synapses can be induced in vivo in the zebrafish and that synaptic patterning is less plastic than synaptic strength during development.

Indexed as

Action PotentialsAnimalsGlutamic AcidMotor NeuronsMuscle, SkeletalNeural PathwaysNeuronal PlasticityReceptors, AMPASwimmingSynapsesSynaptic PotentialsSynaptic TransmissionTumor Necrosis Factor-alphaZebrafishGlutamic AcidReceptors, AMPATumor Necrosis Factor-alpha

Identifiers

PMID20592209
PMCPMC6632878
OpenAlexW2085297861

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.