PMID- 12470709
OWN - NLM
STAT- MEDLINE
DCOM- 20030417
LR  - 20190901
IS  - 0197-0186 (Print)
IS  - 0197-0186 (Linking)
VI  - 42
IP  - 4
DP  - 2003 Mar
TI  - GABA-glutamate interaction in the control of BDNF expression in hypothalamic 
      neurons.
PG  - 353-8
AB  - Brain derived-neurotrophic factor (BDNF) belongs to the neurotrophin family and 
      regulates the survival, differentiation and maintenance of function in different 
      neuronal populations. We previously reported that glutamate increases the 
      expression of BDNF mRNA, its four transcripts and the BDNF peptide in fetal 
      hypothalamic neurons, essentially through NMDA receptor activation. In the 
      present study, we investigated whether GABA interacts with glutamate in the 
      regulation of BDNF gene expression. BDNF and Trk B (BDNF receptor) mRNAs were 
      determined by RNAse protection assay. BDNF transcripts expression levels were 
      evaluated by semi-quantitative RT-PCR. BDNF peptide content was analyzed by 
      enzyme immunoassay (ELISA).We found that picrotoxin (a GABA(A) receptor 
      antagonist) stimulated BDNF mRNA expression and that GABA decreased the 
      glutamate-induced augmentation with no effect on the expression of mRNA encoding 
      the BDNF receptor, Trk B. Measurements of BDNF transcripts levels showed that 
      transcripts containing exons I and III were increased by picrotoxin, whereas 
      those containing exons II and IV were unchanged. GABA solely diminished the 
      glutamate-stimulated expression of transcripts containing exon III. In addition, 
      GABA also inhibited the stimulatory effect of glutamate on BDNF peptide content. 
      Our findings show an interaction between glutamate and GABA on BDNF expression 
      (mRNA, transcripts and peptide) in fetal hypothalamic neurons.
FAU - Marmigere, Frederic
AU  - Marmigere F
AD  - Laboratoire de Plasticite Cerebrale, UMR 5102 CNRS, Universite Montpellier 2, CC 
      090, Place Eugene Bataillon, France.
FAU - Rage, Florence
AU  - Rage F
FAU - Tapia-Arancibia, Lucia
AU  - Tapia-Arancibia L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Neurochem Int
JT  - Neurochemistry international
JID - 8006959
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (GABA Antagonists)
RN  - 0 (RNA, Messenger)
RN  - 124-87-8 (Picrotoxin)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 56-12-2 (gamma-Aminobutyric Acid)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*biosynthesis
MH  - Enzyme-Linked Immunosorbent Assay
MH  - GABA Antagonists/pharmacology
MH  - Glutamic Acid/*physiology
MH  - Hypothalamus/cytology/*metabolism
MH  - Male
MH  - Neurons/*metabolism
MH  - Nuclease Protection Assays
MH  - Picrotoxin/pharmacology
MH  - RNA, Messenger/biosynthesis/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/biosynthesis
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Transcription, Genetic/drug effects
MH  - gamma-Aminobutyric Acid/*physiology
EDAT- 2002/12/10 04:00
MHDA- 2003/04/18 05:00
CRDT- 2002/12/10 04:00
PHST- 2002/12/10 04:00 [pubmed]
PHST- 2003/04/18 05:00 [medline]
PHST- 2002/12/10 04:00 [entrez]
AID - S0197018602001006 [pii]
AID - 10.1016/s0197-0186(02)00100-6 [doi]
PST - ppublish
SO  - Neurochem Int. 2003 Mar;42(4):353-8. doi: 10.1016/s0197-0186(02)00100-6.