Evidence map›Paper›PMID 41812870›Full record

ArticleProgress in neurobiology2026

Spinal motoneuron excitability is homeostatically regulated through β-adrenergic neuromodulation in wild-type and presymptomatic SOD1 mice.

Stefano Antonucci, Guillaume Caron, Natalie Dikwella, Sruthi Sankari Krishnamurthy, Anthony Harster, Bartosz Wasicki, Hina Zarrin, Aboud Tahanis, Florian Olde Heuvel, Simon M Danner and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Progress in neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Chronic Diazepam Reveals Excessive Homeostatic Gain in SOD1International journal of molecular sciences · 2026
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Stefano AntonucciDept. of Neurology, Ulm University, Ulm, DE, Germany.
Guillaume CaronUniversité Paris Cité, CNRS, Saints-Pères Paris Institute for the Neurosciences, Paris, France. Electronic address: guillaume.caron@u-paris.fr.
Natalie DikwellaDept. of Neurology, Ulm University, Ulm, DE, Germany.
Sruthi Sankari KrishnamurthyDept. of Neurology, Ulm University, Ulm, DE, Germany.
Anthony HarsterUniversité Paris Cité, CNRS, Saints-Pères Paris Institute for the Neurosciences, Paris, France.
Bartosz WasickiDept. of Neurobiology, Poznań University of Physical Education, Poland.
Hina ZarrinDept. of Neurology, Ulm University, Ulm, DE, Germany.
Aboud TahanisDept. of Neurology, Ulm University, Ulm, DE, Germany.
Florian Olde HeuvelDept. of Neurology, Ulm University, Ulm, DE, Germany.
Simon M DannerDepartment of Neurobiology and Anatomy, College of Medicine, Drexel University, Philadelphia, United States.
Albert C LudolphDept. of Neurology, Ulm University, Ulm, DE, Germany; German Center for Neurodegenerative Diseases (DZNE), Ulm, DE, Germany.
Kamil GryczDept. of Neurobiology, Poznań University of Physical Education, Poland.
Marcin BączykDept. of Neurobiology, Poznań University of Physical Education, Poland. Electronic address: baczyk@awf.poznan.pl.
Daniel ZytnickiUniversité Paris Cité, CNRS, Saints-Pères Paris Institute for the Neurosciences, Paris, France.
Francesco RoselliDept. of Neurology, Ulm University, Ulm, DE, Germany; German Center for Neurodegenerative Diseases (DZNE), Ulm, DE, Germany. Electronic address: francesco.roselli@uni-ulm.de.

Funding

Propriopsinal neuron function in normal and post-SCI locomotionR01NS112304 · NINDS · UNIVERSITY OF LOUISVILLE · PI Simon Michael Danner, David SK Magnuson · 2021 to 2026
$3.0M
Motoneuron mortality in neurodegenerative diseases induced by homeostatic dysregulation of excitabilityR01NS110953 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BINDER, MARC D, HECKMAN, CHARLES · 2019 to 2023
$2.8M
Spinal circuits for sensorimotor integration and interlimb coordination during locomotionR01NS115900 · NINDS · DREXEL UNIVERSITY · PI DANNER, SIMON MICHAEL · 2020 to 2024
$1.7M
NINDS NIH HHS R01 NS110953NINDS NIH HHS R01 NS112304NINDS NIH HHS R01 NS115900
6 · The paper itself

Abstract

Homeostatic feedback loops are essential to stabilize the activity of neurons and neuronal networks. It has been hypothesized that, in the context of Amyotrophic Lateral Sclerosis (ALS), an excessive gain in feedback loops might hyper- or hypo-excite motoneurons (MNs) and contribute to the pathogenesis. Here, we investigated how the neuromodulation of MN intrinsic properties is homeostatically controlled in presymptomatic adult SOD1(G93A) mice and in the age-matched control WT mice. First, we determined that Adrb2 and Adrb3 adrenergic receptors, which are Gs-coupled receptors and subject to tight and robust feedback loops, are specifically expressed in spinal MNs of both SOD1 and WT mice at P45. We then demonstrated that these receptors elicit a so-far overlooked neuromodulation of the electrical properties of MNs, in particular the frequency-current gain, a crucial determinant of excitability. These electrical properties are homeostatically regulated following receptor engagement, which triggers ion channel transcriptional changes and downregulates those receptors. These homeostatic feedbacks are not dysregulated in presymptomatic SOD1 mice, and they set the MN excitability upon β-adrenergic neuromodulation.

Indexed as

Amyotrophic Lateral SclerosisHomeostasisMotor NeuronsReceptors, Adrenergic, beta-2Receptors, Adrenergic, beta-3Spinal CordAnimalsMiceMice, TransgenicSuperoxide Dismutase-1ADRB2 protein, mouseReceptors, Adrenergic, beta-2Receptors, Adrenergic, beta-3Sod1 protein, mouseSuperoxide Dismutase-1Amyotrophic Lateral SclerosisChannelomeG protein-coupled receptorsHomeostatic regulationin vivo intracellular electrophysiologyTranscriptomicsβ-adrenergic neuromodulation

Identifiers

PMID41812870
PMCPMC13288352

What OpenQuestion holds

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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.