PMID- 11746355
OWN - NLM
STAT- MEDLINE
DCOM- 20020125
LR  - 20131121
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 66
IP  - 3
DP  - 2001 Nov 1
TI  - Regulation of brain-derived neurotrophic factor transcripts by neuronal 
      activation in rat hypothalamic neurons.
PG  - 377-89
AB  - Brain-derived neurotrophic factor (BDNF) belongs to the neurotrophin family and 
      regulates the survival, differentiation, and maintenance of function in different 
      neuronal populations. BDNF is strongly expressed in hypothalamic neurons, where 
      it exerts long- or short-lasting actions. Because glutamate has been associated 
      with regulations of hypothalamic hormones, we examined the regulation of the four 
      promoters of the BDNF gene by glutamate in fetal hypothalamic neurons. The 
      expression levels of BDNF transcripts were investigated using semiquantitative 
      RT-PCR. BDNF protein was determined by enzyme immunoassay, and BDNF and Trk B 
      (BDNF receptor) gene variations were determined by RNAse protection assay. By 
      RT-PCR, we showed that, under basal conditions, BDNF transcripts from exons I, 
      II, and III but not from IV were expressed in the hypothalamic neurons. Glutamate 
      increased expression of both the protein and the four transcripts via 
      N-methyl-D-aspartate receptors, with maximal stimulations after 3 hr of 
      application for exon I and II mRNAs and after 1 hr for exon III and IV mRNAs. 
      Actinomycin D blocked the increase of all transcripts, whereas cycloheximide 
      treatment inhibited stimulation only of exon I and II mRNAs. Trk B mRNA was 
      rapidly and transiently reduced after glutamate application. Our results 
      demonstrate that glutamate 1) regulates BDNF mRNA expression at an early 
      developmental stage in hypothalamic neurons and 2) exerts a differential 
      regulation of BDNF transcripts.
CI  - Copyright 2001 Wiley-Liss, Inc.
FAU - Marmigere, F
AU  - Marmigere F
AD  - Laboratoire de Plasticite Cerebrale, Universite Montpellier 2, Montpellier, 
      France.
FAU - Rage, F
AU  - Rage F
FAU - Tapia-Arancibia, L
AU  - Tapia-Arancibia L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
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 Agonists)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Oligonucleotide Probes)
RN  - 0 (Protein Synthesis Inhibitors)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 3.1.- (Ribonucleases)
SB  - IM
MH  - Aging/metabolism
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*genetics/metabolism
MH  - Cells, Cultured
MH  - Dose-Response Relationship, Drug
MH  - Excitatory Amino Acid Agonists/pharmacology
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Exons/drug effects/genetics
MH  - Fetus
MH  - Gene Expression Regulation, Developmental/drug effects/*physiology
MH  - Glutamic Acid/*metabolism/pharmacology
MH  - Hypothalamus/drug effects/*embryology/*metabolism
MH  - Neurons/drug effects/*metabolism
MH  - Oligonucleotide Probes/pharmacology
MH  - Promoter Regions, Genetic/drug effects/physiology
MH  - Protein Synthesis Inhibitors/pharmacology
MH  - RNA, Messenger/drug effects/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/genetics
MH  - Receptors, N-Methyl-D-Aspartate/agonists/antagonists & inhibitors/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Ribonucleases/analysis
MH  - Time Factors
MH  - Transcription, Genetic/drug effects/physiology
EDAT- 2001/12/18 10:00
MHDA- 2002/01/26 10:01
CRDT- 2001/12/18 10:00
PHST- 2001/12/18 10:00 [pubmed]
PHST- 2002/01/26 10:01 [medline]
PHST- 2001/12/18 10:00 [entrez]
AID - 10.1002/jnr.1230 [pii]
AID - 10.1002/jnr.1230 [doi]
PST - ppublish
SO  - J Neurosci Res. 2001 Nov 1;66(3):377-89. doi: 10.1002/jnr.1230.