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Electroacupuncture restores spatial learning and downregulates phosphorylated N-methyl-D-aspartate receptors in a mouse model of Parkinson's disease
  1. Kung-Wen Lu1,2,
  2. Jun Yang2,
  3. Ching-Liang Hsieh2,3,
  4. Yu-Chan Hsu4,
  5. Yi-Wen Lin4,5
  1. 1College of Chinese Medicine, School of Post-Baccalaureate Chinese Medicine, China Medical University, Taichung, Taiwan
  2. 2Department of Chinese Medicine, China Medical University Hospital, Taichung, Taiwan
  3. 3College of Chinese Medicine, Graduate Institute of Integrative Medicine, China Medical University, Taichung, Taiwan
  4. 4College of Chinese Medicine, Graduate Institute of Acupuncture Science, China Medical University, Taichung, Taiwan
  5. 5Research Center for Chinese Medicine & Acupuncture, China Medical University, Taichung, Taiwan
  1. Correspondence to Professor Yi-Wen Lin, Graduate Institute of Acupuncture Science and Acupuncture Research Center, China Medical University. 91 Hsueh-Shih Road, Taichung 40402, Taiwan; yiwenlin{at}


Objective Parkinson's disease (PD) is a degenerative disorder of the central nervous system. PD can be classified as idiopathic, acquired or hereditary and may be caused by various factors such as oxidative stress, loss of mitochondrial function, neuronal excitotoxicity or calcium imbalance.

Methods We hypothesised that electroacupuncture (EA) at KI3 would reduce neuronal excitotoxicity by regulating N-methyl-D-aspartate (NMDA) receptor function and may represent a novel therapeutic approach for PD.

Results Our results showed that deficits in spatial learning (reflected by the escape latency time in the Morris water maze task) and long-term potentiation (LTP) caused by systemic 6-hydroxydopamine (6-OHDA) administration (that damages dopaminergic neurons) could be rescued by EA on day 3. In PD mice, phosphorylated NMDA receptor subunits NR1 and NR2B were elevated (134.03±10.17% and 123.46±3.47% of baseline levels, respectively) but total NR1 and NR2B was unaffected (101.37±3.87% and 102.61±4.22% of baseline, respectively). Elevated levels of pNR1 and pNR2B, and phosphorylated forms of protein kinase A, protein kinase C, α Ca2+/calmodulin-dependent protein kinase extracellular signal-regulated kinases (pERK), and cAMP response element-binding protein were also reduced following EA.

Conclusions These novel findings suggest that EA can rescue learning and LTP deficits in a rodent model of PD. The results point to a possible role for EA-based approaches in the clinical treatment of learning deficits associated with PD.

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