PMID- 12480178
OWN - NLM
STAT- MEDLINE
DCOM- 20030616
LR  - 20190826
IS  - 0169-328X (Print)
IS  - 0169-328X (Linking)
VI  - 108
IP  - 1-2
DP  - 2002 Dec
TI  - Long-term high-frequency electro-acupuncture stimulation prevents neuronal 
      degeneration and up-regulates BDNF mRNA in the substantia nigra and ventral 
      tegmental area following medial forebrain bundle axotomy.
PG  - 51-9
AB  - Electroacupuncture (EA) has been used in China for many years to treat 
      Parkinson's disease (PD) with reportedly effective results. However, the 
      physiological and biological mechanism behind its effectiveness is still unknown. 
      In the present study, different frequencies of chronic EA stimulation (0, 2, 100 
      Hz) were tested in a partially lesioned rat model of PD which was induced by 
      transection of the medial forebrain bundle (MFB). After 24 sessions of EA 
      stimulation (28 days after MFB transection), dopaminergic neurons in the ventral 
      midbrain were examined by immunohistochemical staining, and brain-derived 
      neurotrophic factor (BDNF) mRNA levels in ventral midbrain were measured by in 
      situ hybridization. The results show a marked decrease of dopaminergic neurons on 
      the lesioned side of the substantia nigra (SN) comparing with the unlesioned 
      side. Zero Hz and 2 Hz EA stimulation had no effect on the disappearance of 
      dopaminergic neurons. However, after 100 Hz EA, about 60% of the tyrosine 
      hydroxylase (TH)-positive neurons remained on the lesioned side of the SN. In 
      addition, levels of BDNF mRNA in the SN and ventral tegmental area (VTA) of the 
      lesioned side were significantly increased in the 100 Hz EA group, but unchanged 
      in the 0 and 2 Hz groups. Our results suggest that long-term high-frequency EA is 
      effective in halting the degeneration of dopaminergic neurons in the SN and 
      up-regulating the levels of BDNF mRNA in the subfields of the ventral midbrain. 
      Activation of endogenous neurotrophins by EA may be involved in the regeneration 
      of the injured dopaminergic neurons, which may underlie the effectiveness of EA 
      in the treatment of PD.
FAU - Liang, Xi-Bin
AU  - Liang XB
AD  - Neuroscience Research Institute, Peking University, 38 Xueyuan Road, Beijing 
      100083, PR China.
FAU - Liu, Xian-Yu
AU  - Liu XY
FAU - Li, Feng-Qiao
AU  - Li FQ
FAU - Luo, Yong
AU  - Luo Y
FAU - Lu, Jun
AU  - Lu J
FAU - Zhang, Wang-Ming
AU  - Zhang WM
FAU - Wang, Xiao-Min
AU  - Wang XM
FAU - Han, Ji-Sheng
AU  - Han JS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res Mol Brain Res
JT  - Brain research. Molecular brain research
JID - 8908640
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (RNA, Messenger)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Axotomy
MH  - Brain-Derived Neurotrophic Factor/*genetics/metabolism
MH  - China
MH  - Disease Models, Animal
MH  - Dopamine/metabolism
MH  - Electroacupuncture/*methods
MH  - Female
MH  - Humans
MH  - In Situ Hybridization
MH  - Medial Forebrain Bundle/*surgery
MH  - Neurons/chemistry/metabolism
MH  - Parkinson Disease/therapy
MH  - RNA, Messenger/*metabolism
MH  - Random Allocation
MH  - Rats
MH  - Substantia Nigra/cytology/*metabolism
MH  - Tyrosine 3-Monooxygenase/metabolism
MH  - Up-Regulation/physiology
MH  - Ventral Tegmental Area/cytology/*metabolism
EDAT- 2002/12/14 04:00
MHDA- 2003/06/17 05:00
CRDT- 2002/12/14 04:00
PHST- 2002/12/14 04:00 [pubmed]
PHST- 2003/06/17 05:00 [medline]
PHST- 2002/12/14 04:00 [entrez]
AID - S0169328X02005132 [pii]
AID - 10.1016/s0169-328x(02)00513-2 [doi]
PST - ppublish
SO  - Brain Res Mol Brain Res. 2002 Dec;108(1-2):51-9. doi: 
      10.1016/s0169-328x(02)00513-2.