Acupuncture prevents 6-hydroxydopamine-induced neuronal death in the nigrostriatal dopaminergic system in the rat Parkinson's disease model

Exp Neurol. 2003 Mar;180(1):93-8. doi: 10.1016/s0014-4886(02)00031-6.

Abstract

Parkinson's disease (PD) is a chronic neurodegenerative disorder, and it has been suggested that treatments promoting survival and functional recovery of affected dopaminergic neurons could have a significant and long-term therapeutic value. In the present study, we investigated the neuroprotective effects of acupuncture on the nigrostriatal system in rat unilaterally lesioned with 6-hydroxydopamine (6-OHDA, 4 microg/microl, intrastriatal injection) using tyrosine hydroxylase (TH) and receptor for brain-derived neurotrophic factor, trkB, immunohistochemistries. Two weeks after the lesions were made, rats presented with asymmetry in rotational behavior (118.3 +/- 17.5 turns/h) following injection with apomorphine, a dopamine receptor agonist (0.5 mg/kg, sc). In contrast, acupunctural treatment at acupoints GB34 and LI3 was shown to significantly reduce this motor deficit (14.6 +/- 13.4 turns/h). Analysis via TH immunohistochemistry revealed a substantial loss of cell bodies in the substantia nigra (SN) (45.7% loss) and their terminals in the dorsolateral striatum ipsilateral to the 6-OHDA-induced lesion. However, acupunctural treatment resulted in the enhanced survival of dopaminergic neurons in the SN (21.4% loss) and their terminals in the dorsolateral striatum. Acupuncture also increased the expression of trkB significantly (35.6% increase) in the ipsilateral SN. In conclusion, we observed that only acupuncturing without the use of any drug has the neuroprotective effects against neuronal death in the rat PD model and these protective properties of acupuncture could be mediated by trkB.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acupuncture Therapy* / methods
  • Animals
  • Apomorphine / pharmacology
  • Behavior, Animal / drug effects
  • Cell Count
  • Cell Survival
  • Corpus Striatum / metabolism*
  • Corpus Striatum / pathology
  • Disease Models, Animal
  • Dopamine / metabolism
  • Immunohistochemistry
  • Male
  • Motor Activity / drug effects
  • Neurons / metabolism*
  • Neurons / pathology
  • Oxidopamine
  • Parkinson Disease, Secondary / chemically induced
  • Parkinson Disease, Secondary / pathology
  • Parkinson Disease, Secondary / therapy*
  • Rats
  • Rats, Sprague-Dawley
  • Receptor, trkB / biosynthesis
  • Substantia Nigra / metabolism*
  • Substantia Nigra / pathology
  • Tyrosine 3-Monooxygenase / biosynthesis

Substances

  • Oxidopamine
  • Tyrosine 3-Monooxygenase
  • Receptor, trkB
  • Apomorphine
  • Dopamine