Evidence map›Paper›PMID 21832030›Full record

ArticleJournal of neurophysiology2011

Permanent central synaptic disconnection of proprioceptors after nerve injury and regeneration. II. Loss of functional connectivity with motoneurons.

Katie L Bullinger, Paul Nardelli, Martin J Pinter, Francisco J Alvarez, Timothy C Cope

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
2.0field-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

56 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Delayed-Onset Muscle Soreness Begins with a Transient Neural Switch.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Biophysical model of muscle spindle encoding.Experimental physiology · 2024
    Review
  8. Article
  9. Article
  10. Structural Preservation Does Not Ensure Function at Sensory Ia-Motoneuron Synapses following Peripheral Nerve Injury and Repair.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. CD3International journal of molecular sciences · 2022
    Article
  16. Review
  17. Article
  18. Review
  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.

Katie L BullingerDept. of Neuroscience, Cell Biology, and Physiology, Wright State Univ. School of Medicine, 3640 Colonel Glenn Hwy., Dayton OH 45435, USA.
Paul Nardelli
Martin J Pinter
Francisco J Alvarez
Timothy C Cope
Wright State University · USEmory 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
DEVELOPMENT OF SYNAPTIC INPUTS ON SPINAL INTERNEURONSR01NS047357 · NINDS · WRIGHT STATE UNIVERSITY · PI ALVAREZ, FRANCISCO J · 2004 to 2025
$6.4M
NINDS NIH HHS P01 NS057228NINDS NIH HHS P01-NS-057228NINDS NIH HHS R01 NS047357
6 · The paper itself

Abstract

Regeneration of a cut muscle nerve fails to restore the stretch reflex, and the companion paper to this article [Alvarez FJ, Titus-Mitchell HE, Bullinger KL, Kraszpulski M, Nardelli P, Cope TC. J Neurophysiol (August 10, 2011). doi:10.1152/jn.01095.2010] suggests an important central contribution from substantial and persistent disassembly of synapses between regenerated primary afferents and motoneurons. In the present study we tested for physiological correlates of synaptic disruption. Anesthetized adult rats were studied 6 mo or more after a muscle nerve was severed and surgically rejoined. We recorded action potentials (spikes) from individual muscle afferents classified as IA like (*IA) by several criteria and tested for their capacity to produce excitatory postsynaptic potentials (EPSPs) in homonymous motoneurons, using spike-triggered averaging (STA). Nearly every paired recording from a *IA afferent and homonymous motoneuron (93%) produced a STA EPSP in normal rats, but that percentage was only 17% in rats with regenerated nerves. In addition, the number of motoneurons that produced aggregate excitatory stretch synaptic potentials (eSSPs) in response to stretch of the reinnervated muscle was reduced from 100% normally to 60% after nerve regeneration. The decline in functional connectivity was not attributable to synaptic depression, which returned to its normally low level after regeneration. From these findings and those in the companion paper, we put forward a model in which synaptic excitation of motoneurons by muscle stretch is reduced not only by misguided axon regeneration that reconnects afferents to the wrong receptor type but also by retraction of synapses with motoneurons by spindle afferents that successfully reconnect with spindle receptors in the periphery.

Indexed as

Action PotentialsAnimalsAxonsCell CommunicationExcitatory Postsynaptic PotentialsFemaleMotor NeuronsMuscle, SkeletalMuscle SpindlesNerve RegenerationNeurons, AfferentPeripheral Nerve InjuriesProprioceptionRatsRats, WistarRecovery of Function

Identifiers

PMID21832030
PMCPMC3214087
OpenAlexW2082337750

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.