PMID- 19326433
OWN - NLM
STAT- MEDLINE
DCOM- 20090831
LR  - 20220331
IS  - 1097-4547 (Electronic)
IS  - 0360-4012 (Linking)
VI  - 87
IP  - 10
DP  - 2009 Aug 1
TI  - NMDA receptors mediate an early up-regulation of brain-derived neurotrophic 
      factor expression in substantia nigra in a rat model of presymptomatic 
      Parkinson's disease.
PG  - 2308-18
LID - 10.1002/jnr.22063 [doi]
AB  - The clinical symptoms of Parkinson's disease (PD) appear late and only when the 
      degenerative process at the level of the nigrostriatal dopamine (DA) pathway is 
      quite advanced. An increase in brain-derived neurotrophic factor (BDNF) 
      expression may be one of the molecular signals associated to compensatory and 
      plastic responses occurring in basal ganglia during presymptomatic PD. In the 
      present study, we used in vivo microdialysis, semiquantitative reverse 
      transcriptase-polymerase chain reaction, and immunohistochemistry to study 
      N-methyl-D-aspartic acid (NMDA) receptor regulation of BDNF expression in 
      substantia nigra (SN) of adult rats after partial lesioning of the nigrostriatal 
      DA pathway with unilateral striatal injections of 6-hydroxydopamine (6-OHDA). A 
      time-dependent partial decrease of striatal DA tissue content as well as parallel 
      and gradual increases in extracellular glutamate and aspartate levels in SN were 
      found 1 to 7 days after unilateral 6-OHDA intrastriatal injection. Instead, the 
      number of tyrosine hydroxylase-immunoreactive (IR) cells in the ipsilateral SN 
      pars compacta remained statistically unchanged after neurotoxin injection. 
      Intrastriatal administration of 6-OHDA also produced an early and transient 
      augmentation of pan-BDNF, exon II-BDNF, and exon III-BDNF transcripts in the 
      ipsilateral SN. The pan-BDNF and exon II-BDNF transcript increases were 
      completely abolished by the prior systemic administration of MK-801, a selective 
      antagonist of NMDA receptors. MK-801 also blocked the increase in BDNF-IR cells 
      in SN observed 7 days after unilateral 6-OHDA intrastriatal injections. Our 
      findings suggest that a coupling between glutamate release, NMDA receptor 
      activation, and BDNF expression may exist in the adult SN and represent an 
      important signal in this midbrain nucleus triggered in response to partial DA 
      loss occurring in striatal nerve endings during presymptomatic PD.
CI  - Copyright 2009 Wiley-Liss, Inc.
FAU - Bustos, Gonzalo
AU  - Bustos G
AD  - Laboratory of Biochemical Pharmacology, Department of Cell and Molecular Biology, 
      Faculty of Biological Sciences, Pontificia Universidad Catolica de Chile, 
      Santiago, Chile. gbustos@bio.puc.cl
FAU - Abarca, Jorge
AU  - Abarca J
FAU - Bustos, Victor
AU  - Bustos V
FAU - Riquelme, Eduardo
AU  - Riquelme E
FAU - Noriega, Viviana
AU  - Noriega V
FAU - Moya, Catherine
AU  - Moya C
FAU - Campusano, Jorge
AU  - Campusano J
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 30KYC7MIAI (Aspartic Acid)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 6LR8C1B66Q (Dizocilpine Maleate)
RN  - 8HW4YBZ748 (Oxidopamine)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Aspartic Acid/metabolism
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism
MH  - Cell Count/methods
MH  - Disease Models, Animal
MH  - Dizocilpine Maleate/pharmacology
MH  - Dopamine/metabolism
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Functional Laterality
MH  - Glutamic Acid/metabolism
MH  - Male
MH  - Microdialysis/methods
MH  - Oxidopamine
MH  - Parkinson Disease, Secondary/chemically induced/*pathology
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, N-Methyl-D-Aspartate/*physiology
MH  - Substantia Nigra/*metabolism
MH  - Time Factors
MH  - Tyrosine 3-Monooxygenase/metabolism
MH  - Up-Regulation/drug effects/*physiology
EDAT- 2009/03/28 09:00
MHDA- 2009/09/01 06:00
CRDT- 2009/03/28 09:00
PHST- 2009/03/28 09:00 [entrez]
PHST- 2009/03/28 09:00 [pubmed]
PHST- 2009/09/01 06:00 [medline]
AID - 10.1002/jnr.22063 [doi]
PST - ppublish
SO  - J Neurosci Res. 2009 Aug 1;87(10):2308-18. doi: 10.1002/jnr.22063.