中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (8): 3533-3534.doi: 10.4103/NRR.NRR-D-25-00176

• 观点:退行性病与再生 • 上一篇    下一篇

左旋多巴诱导运动障碍的运动皮质:亚麻醉氯胺酮治疗后系统和分子变化

  

  • 出版日期:2026-08-18 发布日期:2026-04-25

Motor cortex in levodopa-induced dyskinesia: systems and molecular changes after sub-anesthetic ketamine treatment

Torsten Falk, Stephen L. Cowen*   

  1. Psychology Department, The University of Arizona, Tucson, AZ, USA (Cowen SL)
    Department of Neurology and Department of Pharmacology, The University of Arizona, Tucson, AZ, USA (Falk T)
  • Online:2026-08-18 Published:2026-04-25
  • Contact: Stephen L. Cowen, PhD, scowen@arizona.edu.
  • Supported by:
    This work was supported by Arizona Biomedical Research Commission [ADHS18-198846], the National Institute of Health NINDS [R56-NS109608 and R01-NS122805], and Davies, Robert and Peyton, Parkinson’s Disease Research Fund to TF.

摘要: https://orcid.org/0000-0002-7733-1559 (Stephen L. Cowen)

Abstract: The loss of control over movement is one of the most devastating consequences of Parkinson’s disease (PD). The loss of control largely results from the gradual but inexorable destruction of dopamine-producing neurons in the substantia nigra pars compacta. As dopamine levels fall, the ability to initiate, control, learn, and sustain actions declines. Treatment with the dopamine precursor levodopa can partly overcome motor impairments; however, years of use often leads to levodopa-induced dyskinesia (LID), a debilitating condition characterized by uncontrolled writhing and ballistic movements, making continued treatment difficult or impossible. While progress has been made towards unraveling the molecular and cellular processes driving the development of LID, far less is known about the changes in ongoing neuronal activity that contribute to LID expression.