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<p>Neuronal gap junctions, or electrical synapses, are extensively expressed in the mammalian forebrain and play a key role in synchronizing network activity. Connexin 36 (<b>Cx36</b>) 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 (<b>KO</b>) 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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月25日

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  • James M. McNally,
  • Sean Carey,
  • David S. Uygun,
  • Stephen Thankachan,
  • Radhika Basheer

摘要

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.