Evidence map›Paper›PMID 28543879›Full record

ArticleThe Journal of comparative neurology2017

VGLUT1 synapses and P-boutons on regenerating motoneurons after nerve crush.

Adam J Schultz, Travis M Rotterman, Anirudh Dwarakanath, Francisco J Alvarez

Open access · greenAbstract read
In one paragraph

Article in The Journal of comparative neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.6field-weighted citation impact, top 39% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

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  14. Spinal Motor Circuit Synaptic Plasticity after Peripheral Nerve Injury Depends on Microglia Activation and a CCR2 Mechanism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
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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

4 authors at 1 institution in 1 country.

Adam J SchultzDepartment of Physiology, Emory University, Atlanta, Georgia.
Travis M RottermanDepartment of Physiology, Emory University, Atlanta, Georgia.
Anirudh DwarakanathDepartment of Physiology, Emory University, Atlanta, Georgia.
Francisco J AlvarezDepartment of Physiology, Emory University, Atlanta, Georgia.ORCID http://orcid.org/0000-0001-7011-3244
Emory University · US

Funding

Synaptic Function: Effects of the Nerve Injury, Repair, and Altered ActivityP01NS057228 · NINDS · WRIGHT STATE UNIVERSITY · PI COPE, TIMOTHY C · 2007 to 2017
$9.1M
ENNCF - Viral Vector CoreP30NS055077 · NINDS · EMORY UNIVERSITY · PI LEVEY, ALLAN I · 2008 to 2018
$6.8M
The involvement of microglia and peripheral macrophages in the permanent deletion of proprioceptive IA afferents from spinal motoneurons following peripheral nerve injuryF31NS095528 · NINDS · EMORY UNIVERSITY · PI ROTTERMAN, TRAVIS MICHAEL · 2015 to 2018
$108k
NINDS NIH HHS F31 NS095528NINDS NIH HHS P01 NS057228NINDS NIH HHS P30 NS055077
6 · The paper itself

Abstract

Stretch-sensitive Ia afferent monosynaptic connections with motoneurons form the stretch reflex circuit. After nerve transection, Ia afferent synapses and stretch reflexes are permanently lost, even after regeneration and reinnervation of muscle by motor and sensory afferents is completed in the periphery. This loss greatly affects full recovery of motor function. However, after nerve crush, reflex muscle forces during stretch do recover after muscle reinnervation and reportedly exceed 140% baseline values. This difference might be explained by structural preservation after crush of Ia afferent synapses on regenerating motoneurons and decreased presynaptic inhibitory control. We tested these possibilities in rats after crushing the tibial nerve (TN), and using Vesicular GLUtamate Transporter 1 (VGLUT1) and the 65 kDa isoform of glutamic acid-decarboxylase (GAD65) as markers of, respectively, Ia afferent synapses and presynaptic inhibition (P-boutons) on retrogradely labeled motoneurons. We analyzed motoneurons during regeneration (21 days post crush) and after they reinnervate muscle (3 months). The results demonstrate a significant loss of VGLUT1 terminals on dendrites and cell bodies at both 21 days and 3 months post-crush. However, in both cellular compartments, the reductions were small compared to those observed after TN full transection. In addition, we found a significant decrease in the number of GAD65 P-boutons per VGLUT1 terminal and their coverage of VGLUT1 boutons. The results support the hypothesis that better preservation of Ia afferent synapses and a change in presynaptic inhibition could contribute to maintain or even increase the stretch reflex after nerve crush and by difference to nerve transection.

Indexed as

Analysis of VarianceAnimalsCell CountCholera ToxinDisease Models, AnimalFemaleGene Expression RegulationGlutamate DecarboxylaseMotor NeuronsNerve CrushNerve RegenerationPeripheral Nerve InjuriesPresynaptic TerminalsRatsRats, WistarSynapsesCholera ToxinGlutamate Decarboxylaseglutamate decarboxylase 2Vesicular Glutamate Transport Protein 1glutamic acid decarboxylaseperipheral nerve injurypresynaptic terminalsproprioceptive disordersratsreflexRRID: AB_ 2313637RRID: AB_2315776RRID: AB_2340411RRID: AB_ 2340819RRID: AB_528264RRID: AB_887875RRID: nif_0000_00313RRID: nif-0000-00314RRID: nif_0000_10294stretchWistar

Identifiers

PMID28543879
PMCPMC8063217
OpenAlexW2620535525

What OpenQuestion holds

Textmetadata
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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.