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<p>Parkinson’s disease (PD) is a movement disorder characterized by alpha-synuclein (a-Syn) aggregation, dopaminergic degeneration, and pathological beta oscillations (13–30 Hz) in the basal ganglia circuit. Deep brain stimulation (DBS) is an effective neurosurgical treatment for the motor symptoms of PD. However, the extent to which mitigation of beta oscillations mediates DBS therapeutic effects remains uncertain. Using an adeno-associated virus-mediated nigral A53T a-Syn overexpression rat model, we examined basal ganglia-thalamo-cortical electrophysiology and the model’s responsiveness to DBS. In vivo recordings revealed early beta emergence in the motor cortex (MCx), spreading to the subthalamic nucleus (STN) and entopeduncular nucleus (EP) with neurodegeneration. This was accompanied by alterations in STN and EP single-unit activity. Awake-state beta oscillations manifested as transient bursts. Low- and high-frequency DBS differentially modulated beta bursts and motor performance. Our results demonstrate that the A53T a-Syn model replicates key PD-like electrophysiological features, providing a platform to investigate DBS mechanisms and optimize therapies targeting aberrant beta activity.</p>

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Cortical and basal ganglia beta oscillations and frequency-dependent DBS effects in the A53T Parkinson’s disease rat model

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月19日

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  • Laura Kondrataviciute,
  • Minesh Kapadia,
  • Ivan Skelin,
  • Srdjan Sumarac,
  • Luka Zivkovic,
  • Luis Antonio Franco Vergara,
  • Sabika Jafri,
  • Cherisse Tan,
  • Hien Chau,
  • Yuhan Hou,
  • Savanna Blade,
  • Xilin Liu,
  • Clement Hamani,
  • Taufik Valiante,
  • William D. Hutchison,
  • Luka Milosevic,
  • Lorraine V. Kalia,
  • Suneil K. Kalia

摘要

Parkinson’s disease (PD) is a movement disorder characterized by alpha-synuclein (a-Syn) aggregation, dopaminergic degeneration, and pathological beta oscillations (13–30 Hz) in the basal ganglia circuit. Deep brain stimulation (DBS) is an effective neurosurgical treatment for the motor symptoms of PD. However, the extent to which mitigation of beta oscillations mediates DBS therapeutic effects remains uncertain. Using an adeno-associated virus-mediated nigral A53T a-Syn overexpression rat model, we examined basal ganglia-thalamo-cortical electrophysiology and the model’s responsiveness to DBS. In vivo recordings revealed early beta emergence in the motor cortex (MCx), spreading to the subthalamic nucleus (STN) and entopeduncular nucleus (EP) with neurodegeneration. This was accompanied by alterations in STN and EP single-unit activity. Awake-state beta oscillations manifested as transient bursts. Low- and high-frequency DBS differentially modulated beta bursts and motor performance. Our results demonstrate that the A53T a-Syn model replicates key PD-like electrophysiological features, providing a platform to investigate DBS mechanisms and optimize therapies targeting aberrant beta activity.