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Acetylcholine enhances deviance detection in Hodgkin-Huxley neuronal networks.

Overview

Authors: Fei Fang1,2, Zi-Gang Huang1, Zenas C. Chao2
  1. Key Laboratory of Biomedical Information Engineering of Ministry of Education, Institute of Health and Rehabilitation Science, School of Life Science and Technology, Xi’an Jiaotong University,Xi’an, 710049 China
  2. International Research Center for Neurointelligence (WPI-IRCN), UTIAS, The University of Tokyo,Tokyo, Japan
Institutions: Xi'an Jiaotong University (China); The University of Tokyo (Japan)
Journal: Cognitive neurodynamics, volume 20, issue 1, article 153
Dates: received 18 January 2026; accepted 20 July 2026; published online 7 August 2026; in print December 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.1007/s11571-026-10522-3 · PMID 42571115 · PMCID PMC13451467 · OpenAlex W4413176041
Open access: hybrid, a free copy (OpenAlex)
Status: code verified
Categories: computational modeling (no new data) (modality), none (in silico) (organism), computational (subfield)
Methods: Connectivity, Single-unit activity, calcium imaging
Keywords: Neuromodulator, Deviance detection, Hodgkin-Huxley, Acetylcholine
Topic: Nicotinic Acetylcholine Receptors Study (Molecular Biology, Biochemistry, Genetics and Molecular Biology), according to OpenAlex
Funding: University of Tokyo
Citations: not cited yet (Europe PMC); 75 references in the paper

Abstract

The brain’s ability to detect unexpected events, deviance detection (DD), is critical for survival. While DD has been computationally explained by synaptic plasticity, the role of neuromodulators such as acetylcholine (ACh) remains less understood. Here, we examine how ACh modulates DD. Using a cholinergic-sensitive Hodgkin-Huxley network of 200 neurons arranged in 2D space and stimulated via five spatially distinct inputs (A–E), we implemented an oddball paradigm with three conditions: standard (80% A, 20% B), deviant (20% A, 80% B), and a multi-standard control (20% each of A–E). ACh levels were modeled by varying the conductance of a slow K⁺ current, reflecting cholinergic modulation of the M-current. In the absence of ACh, the network already exhibited DD, responding more strongly to deviant A compared to control A. Notably, introducing a small amount of ACh amplified DD, while further increases suppressed it. Maximal DD occurred when strong spike frequency adaptation to standard B reduced competition, and enhanced phase-locking synchronized the network’s response to deviant A. These findings reveal how neuromodulation can shape context-sensitive neural computation, optimizing detection of salient events through a dynamic balance of suppression and synchronization.

Supplementary Information: The online version contains supplementary material available at 10.1007/s11571-026-10522-3.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

No file of the authors' code could be read here: it is described below, and read at its source.

Zenodo 17072341

License: MIT
State: the link answers, verified on 27 September 2026
Evidence: files inventoried
Size: 0 files, 0 scripts
Software Heritage: not checked
Found in: “Code availability”
Not found: README, license file, CITATION.cff, environment file, tests, continuous integration, documentation
Availability: 1 check, the latest on 27 September 2026: the link answers (HTTP 200)
  • 27 September 2026: the link answers (HTTP 200)
At the source:

Code availability

The source code for our computational model and analysis scripts is publicly available in the Zenodo repository under the DOI: 10.5281/zenodo.17072341.

Reproduced under the paper's license (CC BY), from the paper cited above.

Tracing map

Proposed by the machine: these links were found in the paper and verified at the source, without human review. The map will receive a Zenodo DOI once one of the paper's authors has validated it with their ORCID.

What the map holds:

  • 1 repository of the authors' code, each at its verified commit, with its license and how the link was found in the paper;
  • 0 scripts, each with its path and the digest of its content;
  • no match between paragraphs and code yet;
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Its JSON (tracing-map.json) is deposited on Zenodo with its DOI once the map is validated.

Data

No dataset and no data link were found in the paper.

Data availability

All data used to produce the figureswas generated via numerical simulations of the code, which is publicly available in the Zenodo repository under the DOI: 10.5281/zenodo.17072341.

Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

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Version 1, 27 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 3 authors, 4 keywords, 1 funder, 74 references.

Cite

This paper

Fang, F., Huang, Z.-G., & Chao, Z. C. (2026). Acetylcholine enhances deviance detection in Hodgkin-Huxley neuronal networks. Cognitive neurodynamics, 20(1), 153. https://doi.org/10.1007/s11571-026-10522-3

BibTeX

@article{fang2026acetylcholine,
author = {Fang, Fei and Huang, Zi-Gang and Chao, Zenas C.},
title = {{Acetylcholine enhances deviance detection in Hodgkin-Huxley neuronal networks}},
journal = {Cognitive neurodynamics},
year = {2026},
month = aug,
volume = {20},
number = {1},
pages = {153},
publisher = {Springer},
issn = {1871-4080},
doi = {10.1007/s11571-026-10522-3},
url = {https://doi.org/10.1007/s11571-026-10522-3},
pmid = {42571115},
pmcid = {PMC13451467}
}

RIS

TY - JOUR
AU - Fang, Fei
AU - Huang, Zi-Gang
AU - Chao, Zenas C.
TI - Acetylcholine enhances deviance detection in Hodgkin-Huxley neuronal networks
T2 - Cognitive neurodynamics
J2 - Cogn Neurodyn
PY - 2026
DA - 2026/08/07
VL - 20
IS - 1
SP - 153
SN - 1871-4080
PB - Springer
DO - 10.1007/s11571-026-10522-3
UR - https://doi.org/10.1007/s11571-026-10522-3
LA - en
ER -

CSL-JSON

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The tracing map gets a citation of its own once an author has validated it and it has a DOI.

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