Evidence map›Paper›PMID 25100585›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Presynaptic NCAM is required for motor neurons to functionally expand their peripheral field of innervation in partially denervated muscles.

Peter H Chipman, Melitta Schachner, Victor F Rafuse

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. 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
2.1field-weighted citation impact, top 15% 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, 45 citations in OpenAlex.

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  7. L-type CaCellular and molecular neurobiology · 2022
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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 2 countries.

Peter H ChipmanDepartments of Medical Neuroscience and.
Melitta SchachnerKeck Center for Collaborative Neuroscience, Rutgers University, Piscataway, New Jersey 08854-8082.
Victor F RafuseDepartments of Medical Neuroscience and Medicine (Neurology), Dalhousie University, Halifax, Nova Scotia B3H 1X5, Canada, Brain Repair Centre, Life Science Research Institute, Halifax, Nova Scotia B3H 4H7, Canada, and vrafuse@dal.ca.
Dalhousie University · CARutgers, The State University of New Jersey · US

Funding

Canadian Institutes of Health Research 108413
6 · The paper itself

Abstract

The function of neural cell adhesion molecule (NCAM) expression in motor neurons during axonal sprouting and compensatory reinnervation was explored by partially denervating soleus muscles in mice lacking presynaptic NCAM (Hb9(cre)NCAM(flx)). In agreement with previous studies, the contractile force of muscles in wild-type (NCAM(+/+)) mice recovered completely 2 weeks after 75% of the motor innervation was removed because motor unit size increased by 2.5 times. In contrast, similarly denervated muscles in Hb9(cre)NCAM(flx) mice failed to recover the force lost due to the partial denervation because motor unit size did not change. Anatomical analysis indicated that 50% of soleus end plates were completely denervated 1-4 weeks post-partial denervation in Hb9(cre)NCAM(flx) mice, while another 25% were partially reinnervated. Synaptic vesicles (SVs) remained at extrasynaptic regions in Hb9(cre)NCAM(flx) mice rather than being distributed, as occurs normally, to newly reinnervated neuromuscular junctions (NMJs). Electrophysiological analysis revealed two populations of NMJs in partially denervated Hb9(cre)NCAM(flx) soleus muscles, one with high (mature) quantal content, and another with low (immature) quantal content. Extrasynaptic SVs in Hb9(cre)NCAM(flx) sprouts were associated with L-type voltage-dependent calcium channel (L-VDCC) immunoreactivity and maintained an immature, L-VDCC-dependent recycling phenotype. Moreover, acute nifedipine treatment potentiated neurotransmission at newly sprouted NMJs, while chronic intraperitoneal treatment with nifedipine during a period of synaptic consolidation enhanced functional motor unit expansion in the absence of presynaptic NCAM. We propose that presynaptic NCAM bridges a critical link between the SV cycle and the functional expansion of synaptic territory through the regulation of L-VDCCs.

Indexed as

Muscle DenervationAnimalsCalcium Channel BlockersCalcium Channels, L-TypeCD24 AntigenCholera ToxinExcitatory Postsynaptic PotentialsHomeodomain ProteinsMiceMice, TransgenicMotor NeuronsMuscle ContractionNerve RegenerationNerve Tissue ProteinsNeural Cell Adhesion MoleculesNeuromuscular JunctionCalcium Channel BlockersCalcium Channels, L-TypeCD24 AntigenCd24a protein, mouseCholera ToxinHb9 protein, mouseHomeodomain ProteinsNerve Tissue ProteinsNeural Cell Adhesion Moleculesomega-Agatoxin IVATranscription FactorsNCAMneuromuscular junctionpartial denervationregenerationsprouting

Identifiers

PMID25100585
PMCPMC4122797
OpenAlexW1979511261

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.