Acupuncture enhances the synaptic dopamine availability to improve motor function in a mouse model of Parkinson's disease

PLoS One. 2011;6(11):e27566. doi: 10.1371/journal.pone.0027566. Epub 2011 Nov 22.


Parkinson's disease (PD) is caused by the selective loss of dopaminergic neurons in the substantia nigra (SN) and the depletion of striatal dopamine (DA). Acupuncture, as an alternative therapy for PD, has beneficial effects in both PD patients and PD animal models, although the underlying mechanisms therein remain uncertain. The present study investigated whether acupuncture treatment affected dopamine neurotransmission in a PD mouse model using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). We found that acupuncture treatment at acupoint GB34 improved motor function with accompanying dopaminergic neuron protection against MPTP but did not restore striatal dopamine depletion. Instead, acupuncture treatment increased dopamine release that in turn, may lead to the enhancement of dopamine availability in the synaptic cleft. Moreover, acupuncture treatment mitigated MPTP-induced abnormal postsynaptic changes, suggesting that acupuncture treatment may increase postsynaptic dopamine neurotransmission and facilitate the normalization of basal ganglia activity. These results suggest that the acupuncture-induced enhancement of synaptic dopamine availability may play a critical role in motor function improvement against MPTP.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
  • Acupuncture Points
  • Acupuncture Therapy*
  • Animals
  • Behavior, Animal
  • Disease Models, Animal
  • Dopamine / metabolism*
  • Dopamine and cAMP-Regulated Phosphoprotein 32 / metabolism
  • Dopaminergic Neurons / metabolism
  • Dopaminergic Neurons / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Models, Biological
  • Motor Activity / physiology*
  • Neostriatum / pathology
  • Neostriatum / physiopathology
  • Nerve Degeneration / complications
  • Nerve Degeneration / pathology
  • Nerve Degeneration / physiopathology
  • Parkinson Disease / physiopathology*
  • Parkinson Disease / therapy*
  • Phosphorylation
  • Proto-Oncogene Proteins c-fos / metabolism
  • Synapses / metabolism*
  • Synapses / pathology
  • Time Factors


  • Dopamine and cAMP-Regulated Phosphoprotein 32
  • Fosb protein, mouse
  • Proto-Oncogene Proteins c-fos
  • 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
  • Dopamine