OSCR

Loss of connexin 36 elicits abnormalities in thalamocortical network activity relevant to neuropsychiatric disorders.

Overview

Authors: James M McNally1, Sean Carey1, David S Uygun1,2, Stephen Thankachan1, Radhika Basheer1
ORCID iDs: James M McNally, David S Uygun, Radhika Basheer
  1. VA Boston Healthcare System and Harvard Medical School, Dept. of Psychiatry, West Roxbury, MA USA
  2. School of Life Sciences, University of Warwick, Coventry, UK
Institutions: Harvard University (United States); VA Boston Healthcare System (United States); University of Warwick (United Kingdom)
Journal: Translational psychiatry, volume 16, issue 1, article 307
Dates: received 17 September 2025; accepted 24 March 2026; published online 25 April 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.1038/s41398-026-04018-1 · PMID 42034628 · PMCID PMC13247216 · OpenAlex W3028755640
Open access: gold, a free copy (OpenAlex)
Status: code on request
Categories: EEG (modality), mouse (organism), schizophrenia / psychosis (population), systems (subfield)
Methods: Statistics, Preprocessing, Spectral & time-frequency, Smoothing, state filtering, decompositions, Physiology & signal measures, Connectivity
Keywords: Physiology, Neuroscience, Schizophrenia
MeSH: Cerebral Cortex*, Connexins*, Thalamus*, Animals, Electroencephalography, Gap Junction delta-2 Protein, Ketamine, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Sleep (* major topic)
Topic: Photoreceptor and optogenetics research (Cellular and Molecular Neuroscience, Neuroscience), according to OpenAlex
Funding: U.S. Department of Veterans Affairs (BX004500, BX002130, BX004905, BX006105); BLRD VA (I01 BX001404, IK2 BX002130, I01 BX006105, I01 BX004500); U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NS119227); U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) (HL007901); U.S. Department of Health & Human Services | NIH | National Institute of Mental Health (NIMH) (MH125242); U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (HL007901); NINDS NIH HHS (R01 NS119227); U.S. Department of Health & Human Services | NIH | National Institute of Mental Health (MH125242); U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) (NS119227)
Citations: cited by 1 paper (Europe PMC); 64 references in the paper

Abstract

Neuronal gap junctions, or electrical synapses, are extensively expressed in the mammalian forebrain and play a key role in synchronizing network activity. Connexin 36 (Cx36) is the primary gap junction protein in mature GABAergic neurons, but its contribution to thalamocortical oscillations and cognitive processes remains unclear. Here, we examined the effects of Cx36 deletion on sleep/wake regulation, spontaneous and evoked EEG activity, and behavior in mice. While Cx36 knockout (KO) mice displayed largely intact sleep architecture, spectral analysis revealed impaired gamma and beta band activity and reduced sigma power surges preceding NREM–REM transitions. Spindle density was preserved, but spindle amplitude and duration were reduced. Cx36KO mice exhibited blunted gamma responses to ketamine, impaired 40 Hz auditory steady-state responses, and reduced mismatch negativity with attenuated ERP amplitudes and altered evoked power. Behaviorally, Cx36KO mice showed impaired social habituation and reduced investigation-induced gamma activity. These findings demonstrate that Cx36-containing gap junctions are essential for maintaining thalamocortical synchrony and support translational EEG biomarkers relevant to schizophrenia and other psychiatric disorders. Cx36 may therefore represent a novel therapeutic target for modulating dysfunctional network activity in neuropsychiatric disease.

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

Code

The paper says that its authors' code is available on request: it was not published with the paper, so there is nothing to verify.

The paper's code and data availability statement is in the Data section.

Tracing map

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Data

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Data availability

All datasets and MATLAB analysis scripts used in this study will be made available upon reasonable request to the corresponding author.

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

Versions

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Version 1, 30 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 5 authors, 3 keywords, 12 MeSH terms, 9 funders, 61 references.

Cite

This paper

McNally, J. M., Carey, S., Uygun, D. S., Thankachan, S., & Basheer, R. (2026). Loss of connexin 36 elicits abnormalities in thalamocortical network activity relevant to neuropsychiatric disorders. Translational psychiatry, 16(1), 307. https://doi.org/10.1038/s41398-026-04018-1

BibTeX

@article{mcnally2026loss,
author = {McNally, James M and Carey, Sean and Uygun, David S and Thankachan, Stephen and Basheer, Radhika},
title = {{Loss of connexin 36 elicits abnormalities in thalamocortical network activity relevant to neuropsychiatric disorders}},
journal = {Translational psychiatry},
year = {2026},
month = apr,
volume = {16},
number = {1},
pages = {307},
publisher = {Nature Publishing Group},
issn = {2158-3188},
doi = {10.1038/s41398-026-04018-1},
url = {https://doi.org/10.1038/s41398-026-04018-1},
pmid = {42034628},
pmcid = {PMC13247216}
}

RIS

TY - JOUR
AU - McNally, James M
AU - Carey, Sean
AU - Uygun, David S
AU - Thankachan, Stephen
AU - Basheer, Radhika
TI - Loss of connexin 36 elicits abnormalities in thalamocortical network activity relevant to neuropsychiatric disorders
T2 - Translational psychiatry
J2 - Transl Psychiatry
PY - 2026
DA - 2026/04/25
VL - 16
IS - 1
SP - 307
SN - 2158-3188
PB - Nature Publishing Group
DO - 10.1038/s41398-026-04018-1
UR - https://doi.org/10.1038/s41398-026-04018-1
LA - en
ER -

CSL-JSON

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