Evidence map›Paper›PMID 37650071›Full record

ArticleFrontiers in cellular neuroscience2023

Neuromuscular recovery from botulism involves multiple forms of compensatory plasticity.

James B Machamer, Edwin J Vazquez-Cintron, Mallory J Stenslik, Kathleen T Pagarigan, Aaron B Bradford, Celinia A Ondeck, Patrick M McNutt

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
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

7 authors at 4 institutions in 1 country.

James B MachamerBASF, Research Triangle Park, NC, United States.
Edwin J Vazquez-CintronUnited States Army Medical Research Institute of Chemical Defense, Gunpowder, MD, United States.
Mallory J StenslikUnited States Army Medical Research Institute of Chemical Defense, Gunpowder, MD, United States.
Kathleen T PagariganUnited States Army Medical Research Institute of Chemical Defense, Gunpowder, MD, United States.
Aaron B BradfordUnited States Army Medical Research Institute of Chemical Defense, Gunpowder, MD, United States.
Celinia A OndeckUnited States Army Medical Research Institute of Chemical Defense, Gunpowder, MD, United States.
Patrick M McNuttUnited States Army Medical Research Institute of Chemical Defense, Gunpowder, MD, United States.
United States Army Medical Research Institute of Infectious Diseases · USForest Institute · USResearch Triangle Park Foundation · USWake Forest University · US

Funding

Novel therapeutic approaches to treatment of botulinum neurotoxin poisoning.R01AI093504 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Konstantin Ichtchenko · 2011 to 2026
$13.9M
Novel therapeutic approaches to treatment of botulinum neurotoxin poisoning.U01AI093504 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ICHTCHENKO, KONSTANTIN · 2019 to 2021
$3.4M
NIAID NIH HHS R01 AI093504NIAID NIH HHS U01 AI093504
6 · The paper itself

Abstract

Introduction: Botulinum neurotoxin (BoNT) causes neuroparalytic disease and death by blocking neuromuscular transmission. There are no specific therapies for clinical botulism and the only treatment option is supportive care until neuromuscular function spontaneously recovers, which can take weeks or months after exposure. The highly specialized neuromuscular junction (NMJ) between phrenic motor neurons and diaphragm muscle fibers is the main clinical target of BoNT. Due to the difficulty in eliciting respiratory paralysis without a high mortality rate, few studies have characterized the neurophysiological mechanisms involved in diaphragm recovery from intoxication. Here, we develop a mouse model of botulism that involves partial paralysis of respiratory muscles with low mortality rates, allowing for longitudinal analysis of recovery. Methods and results: Mice challenged by systemic administration of 0.7 LD Discussion: In addition to identifying multiple forms of compensatory plasticity that occur in response to reduced NMJ function, it is expected that insights into the molecular mechanisms involved in recovery from neuromuscular paralysis will support new host-targeted treatments for multiple neuromuscular diseases.

Indexed as

botulinum neurotoxincompensatory plasticityendplate recordingshemidiaphragm:phrenic nerve preparationsmicerunning wheel activitytwitch and tetanic contractionsvoltage-gated calcium channels

Identifiers

PMID37650071
PMCPMC10463753
OpenAlexW4385874721

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.