PMID- 12853419
OWN - NLM
STAT- MEDLINE
DCOM- 20030807
LR  - 20200225
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 23
IP  - 14
DP  - 2003 Jul 9
TI  - c-fos reduces corticosterone-mediated effects on neurotrophic factor expression 
      in the rat hippocampal CA1 region.
PG  - 6013-22
AB  - The transcription of neurotrophic factors, i.e., basic fibroblast growth factor 
      (bFGF) and brain-derived neurotrophic factor (BDNF) is regulated by 
      glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) activation 
      despite the lack of a classical glucocorticoid response element in their promoter 
      region. A time course for corticosterone (10 mg/kg, s.c.) in adrenalectomized 
      rats revealed a peak hormone effect at the 4 hr time interval for bFGF (110-204% 
      increase), BDNF (53-67% decrease), GR (53-64% decrease), and MR (34-56% decrease) 
      mRNA levels in all hippocampal subregions using in situ hybridization. c-fos mRNA 
      levels were affected exclusively in the dentate gyrus after 50 min to 2 hr 
      (38-46% decrease). Furthermore, it was evaluated whether corticosterone 
      regulation of these genes depends on interactions with the transcription factor 
      complex activator protein-1. c-fos antisense oligodeoxynucleotides were injected 
      into the dorsal hippocampus of adrenalectomized rats. Corticosterone was given 2 
      hr later, and the effects on gene expression were measured 4 hr later. In CA1, 
      antisense treatment significantly and selectively enhanced the hormone action on 
      the expression of bFGF (44% enhanced increase) and BDNF (38% enhanced decrease) 
      versus control oligodeoxynucleotide treatment. In addition, an upregulation of 
      c-fos expression (89% increase) was found. There were no effects of c-fos 
      antisense on hippocampal GR and MR expression. Thus it seems that a tonic c-fos 
      mechanism exists within CA1, which reduces GR- and MR-mediated effects on 
      expression of bFGF and BDNF.
FAU - Hansson, A C
AU  - Hansson AC
AD  - Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden. 
      anita.hansson@neuro.ki.se
FAU - Sommer, W
AU  - Sommer W
FAU - Rimondini, R
AU  - Rimondini R
FAU - Andbjer, B
AU  - Andbjer B
FAU - Stromberg, I
AU  - Stromberg I
FAU - Fuxe, K
AU  - Fuxe K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Biomarkers)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Oligonucleotides, Antisense)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Glucocorticoid)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Adrenalectomy
MH  - Animals
MH  - Biomarkers/analysis
MH  - Corticosterone/blood/*metabolism/pharmacology
MH  - Gene Expression Regulation/drug effects
MH  - Hippocampus/drug effects/*metabolism
MH  - In Situ Hybridization
MH  - Male
MH  - Nerve Growth Factors/genetics/*metabolism
MH  - Oligonucleotides, Antisense/pharmacokinetics/pharmacology
MH  - Proto-Oncogene Proteins c-fos/antagonists & inhibitors/genetics/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Radioimmunoassay
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Glucocorticoid/metabolism
MH  - Stress, Physiological/metabolism
MH  - Tissue Distribution
PMC - PMC6740350
EDAT- 2003/07/11 05:00
MHDA- 2003/08/09 05:00
PMCR- 2004/01/09
CRDT- 2003/07/11 05:00
PHST- 2003/07/11 05:00 [pubmed]
PHST- 2003/08/09 05:00 [medline]
PHST- 2003/07/11 05:00 [entrez]
PHST- 2004/01/09 00:00 [pmc-release]
AID - 23/14/6013 [pii]
AID - 10.1523/JNEUROSCI.23-14-06013.2003 [doi]
PST - ppublish
SO  - J Neurosci. 2003 Jul 9;23(14):6013-22. doi: 10.1523/JNEUROSCI.23-14-06013.2003.