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<p>Effective use of brain-computer interfaces (BCIs) requires the ability to suppress a planned action (volitional inhibition) for adaptable control in real-world scenarios, but their mechanisms are unclear. Here, we used fiber photometry to monitor external globus pallidus (GPe) and subthalamic nucleus (STN) neurons' activity in mice during a volitional stop-signal task (67% GO, 33% NO-GO). GPe/STN neurons (receiving M2 projections) responded to auditory cues, feedback, and rewards in both trials. Importantly, chemogenetic activation of the M2-GPe pathway enhanced volitional inhibition by modulating auditory feedback response, yet inhibited GPe neurons’ feedback response. Furthermore, time-locked optogenetic inhibition of M2-projecting GPe neurons at auditory feedback also enhanced volitional inhibition via prolonged GO trial response times. Collectively, these findings identified the M2-GPe pathway for auditory biofeedback to improve volitional control, offering novel avenues for the advancement of neural interfaces for biofeedback and enhancement of BCI efficacy.</p>

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The Secondary Motor Cortex-External Globus Pallidus Pathway Regulates Auditory Feedback of Volitional Control

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月2日

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  • Shengtao Luo,
  • Yuchen Fan,
  • Feiyang Yu,
  • Xiaopeng Zhou,
  • Ke Hu,
  • Hang Yi,
  • Hui Zhou,
  • Tao Li,
  • Jiang-Fan Chen,
  • Liping Zhang

摘要

Effective use of brain-computer interfaces (BCIs) requires the ability to suppress a planned action (volitional inhibition) for adaptable control in real-world scenarios, but their mechanisms are unclear. Here, we used fiber photometry to monitor external globus pallidus (GPe) and subthalamic nucleus (STN) neurons' activity in mice during a volitional stop-signal task (67% GO, 33% NO-GO). GPe/STN neurons (receiving M2 projections) responded to auditory cues, feedback, and rewards in both trials. Importantly, chemogenetic activation of the M2-GPe pathway enhanced volitional inhibition by modulating auditory feedback response, yet inhibited GPe neurons’ feedback response. Furthermore, time-locked optogenetic inhibition of M2-projecting GPe neurons at auditory feedback also enhanced volitional inhibition via prolonged GO trial response times. Collectively, these findings identified the M2-GPe pathway for auditory biofeedback to improve volitional control, offering novel avenues for the advancement of neural interfaces for biofeedback and enhancement of BCI efficacy.