Evidence map›Paper›PMID 38687681›Full record

ArticleThe Journal of physiology2025

Electrophysiology and 3D-imaging reveal properties of human intracardiac neurons and increased excitability with atrial fibrillation.

J L Ashton, B Prince, G Sands, L Argent, M Anderson, J E G Smith, A Tedoldi, A Ahmad, D Baddeley, A G Pereira and 4 more

Abstract read
In one paragraph

Article in The Journal of physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Autonomic dysregulation and atrial arrhythmias.American journal of physiology. Cell physiology · 2025
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. 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

14 authors.

J L AshtonDepartment of Physiology, University of Auckland, Auckland, New Zealand.ORCID 0000-0003-2376-652X
B PrinceDepartment of Physiology, University of Auckland, Auckland, New Zealand.
G SandsAuckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.ORCID 0000-0002-7875-2099
L ArgentDepartment of Physiology, University of Auckland, Auckland, New Zealand.ORCID 0000-0002-2457-248X
M AndersonCardiothoracic Surgical Unit, Auckland City Hospital, Auckland, New Zealand.
J E G SmithDepartment of Physiology, University of Auckland, Auckland, New Zealand.ORCID 0000-0001-9271-1157
A TedoldiDepartment of Physiology, University of Auckland, Auckland, New Zealand.ORCID 0000-0001-5601-0353
A AhmadDepartment of Physiology, University of Auckland, Auckland, New Zealand.
D BaddeleyAuckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
A G PereiraDepartment of Physiology, University of Auckland, Auckland, New Zealand.ORCID 0000-0002-4068-254X
N LeverManaaki Manawa Centre for Heart Research, University of Auckland and Pūtahi Manawa Centre of Research Excellence, Auckland, New Zealand.
T RamanathanManaaki Manawa Centre for Heart Research, University of Auckland and Pūtahi Manawa Centre of Research Excellence, Auckland, New Zealand.
B H SmaillManaaki Manawa Centre for Heart Research, University of Auckland and Pūtahi Manawa Centre of Research Excellence, Auckland, New Zealand.
Johanna M MontgomeryDepartment of Physiology, University of Auckland, Auckland, New Zealand.

Funding

National Heart Foundation of New Zealand 1887Royal Society New Zealand JCF-UOA2101Royal Society of New Zealand Marsden Fund UOA1801University of Auckland 3726975
6 · The paper itself

Abstract

Altered autonomic input to the heart plays a major role in atrial fibrillation (AF). Autonomic neurons termed ganglionated plexi (GP) are clustered on the heart surface to provide the last point of neural control of cardiac function. To date the properties of GP neurons in humans are unknown. Here we have addressed this knowledge gap in human GP neuron structure and physiology in patients with and without AF. Human right atrial GP neurons embedded in epicardial adipose tissue were excised during open heart surgery performed on both non-AF and AF patients and then characterised physiologically by whole cell patch clamp techniques. Structural analysis was also performed after fixation at both the single cell and at the entire GP levels via three-dimensional confocal imaging. Human GP neurons were found to exhibit unique properties and structural complexity with branched neurite outgrowth. Significant differences in excitability were revealed between AF and non-AF GP neurons as measured by lower current to induce action potential firing, a reduced occurrence of low action potential firing rates, decreased accommodation and increased synaptic density. Visualisation of entire GPs showed almost all neurons are cholinergic with a small proportion of noradrenergic and dual phenotype neurons. Phenotypic distribution differences occurred with AF including decreased cholinergic and dual phenotype neurons, and increased noradrenergic neurons. These data show both functional and structural differences occur between GP neurons from patients with and without AF, highlighting that cellular plasticity occurs in neural input to the heart that could alter autonomic influence on atrial function. KEY POINTS: The autonomic nervous system plays a critical role in regulating heart rhythm and the initiation of AF; however, the structural and functional properties of human autonomic neurons in the autonomic ganglionated plexi (GP) remain unknown. Here we perform the first whole cell patch clamp electrophysiological and large tissue confocal imaging analysis of these neurons from patients with and without AF. Our data show human GP neurons are functionally and structurally complex. Measurements of action potential kinetics show higher excitability in GP neurons from AF patients as measured by lower current to induce action potential firing, reduced low firing action potential rates, and decreased action potential accommodation. Confocal imaging shows increased synaptic density and noradrenergic phenotypes in patients with AF. Both functional and structural differences occur in GP neurons from patients with AF that could alter autonomic influence on atrial rhythm.

Indexed as

Atrial FibrillationCardiac Imaging TechniquesElectrophysiologic Techniques, CardiacImaging, Three-DimensionalNeuronsAgedAged, 80 and overFemaleGanglia, AutonomicHumansMaleMiddle Agedatrial fibrillationelectrophysiologyganglionated plexiintrinsic cardiac nervous systemneurophysiologythree‐dimensional tissue imaging

Identifiers

PMID38687681
PMCPMC11955863

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Registered trials

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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.