PMID- 17967737
OWN - NLM
STAT- MEDLINE
DCOM- 20080117
LR  - 20220311
IS  - 1029-8428 (Print)
IS  - 1029-8428 (Linking)
VI  - 12
IP  - 2
DP  - 2007 Sep
TI  - Brain-derived neurotrophic factor expression in the substantia nigra does not 
      change after lesions of dopaminergic neurons.
PG  - 135-43
AB  - Progressive and irreversible loss of specific neuronal cell populations is 
      commonly seen in chronic neurodegenerative diseases such as Parkinson's disease 
      (PD). Evidence is accumulating that apoptosis is a crucial cellular event 
      responsible for the dysfunction and death of neurons in this disease. Thus, 
      limiting apoptosis may prevent disease pathogenesis. Key to reducing apoptosis is 
      the discovery of neuroprotective compounds that can be given to patients to 
      minimize neuronal damage. In this manuscript, we reviewed the rationale of using 
      an experimental strategy to provide neurotrophic support to injured neurons. Such 
      rationale includes the increase of endogenous production of brain-derived 
      neurotrophic factor (BDNF). BDNF is a potent inhibitor of apoptosis-mediated cell 
      death and neurotoxin-induced degeneration of dopaminergic neurons. However, 
      availability of BDNF may be reduced when dopaminergic neurons degenerate. 
      Therefore, in this work, we have used several well-established neurotoxins for 
      dopaminergic neurons, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, 6-OH-dopamine 
      (6-OHDA), and the HIV protein gp120, to examine whether degeneration of 
      nigrostriatal fibers alters BDNF expression. Our data show that these neurotoxins 
      do not decrease the levels of BDNF in the substantia nigra, suggesting that 
      up-regulation of BDNF synthesis by pharmacological means may be a viable therapy 
      to slow down the progress of PD and other neurodegenerative diseases.
FAU - Mocchetti, Italo
AU  - Mocchetti I
AD  - Department of Neuroscience, Georgetown University Medical Center, Washington DC, 
      USA. moccheti@georgetown.edu
FAU - Bachis, Alessia
AU  - Bachis A
FAU - Nosheny, Rachel L
AU  - Nosheny RL
FAU - Tanda, Gianluigi
AU  - Tanda G
LA  - eng
GR  - NS 040670/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Neurotox Res
JT  - Neurotoxicity research
JID - 100929017
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Neurotoxins)
RN  - 8HW4YBZ748 (Oxidopamine)
RN  - 9P21XSP91P (1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/pharmacology
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Disease Models, Animal
MH  - Dopamine/*metabolism
MH  - Male
MH  - Mice
MH  - Nerve Degeneration/chemically induced
MH  - Neurons/*metabolism/*pathology
MH  - Neurotoxins/toxicity
MH  - Oxidopamine/toxicity
MH  - Parkinson Disease/etiology/*pathology
MH  - Rats
MH  - Substantia Nigra/*pathology
MH  - Time Factors
MH  - Tyrosine 3-Monooxygenase/metabolism
EDAT- 2007/10/31 09:00
MHDA- 2008/01/18 09:00
CRDT- 2007/10/31 09:00
PHST- 2007/10/31 09:00 [pubmed]
PHST- 2008/01/18 09:00 [medline]
PHST- 2007/10/31 09:00 [entrez]
AID - 10.1007/BF03033922 [doi]
PST - ppublish
SO  - Neurotox Res. 2007 Sep;12(2):135-43. doi: 10.1007/BF03033922.