PMID- 19020498
OWN - NLM
STAT- MEDLINE
DCOM- 20090617
LR  - 20151119
IS  - 1740-634X (Electronic)
IS  - 0893-133X (Linking)
VI  - 34
IP  - 6
DP  - 2009 May
TI  - Acute stress responsiveness of the neurotrophin BDNF in the rat hippocampus is 
      modulated by chronic treatment with the antidepressant duloxetine.
PG  - 1523-32
LID - 10.1038/npp.2008.208 [doi]
AB  - Compelling evidence suggests that mood disorders are characterized by reduced 
      neuronal plasticity that might be normalized by pharmacological intervention. Our 
      study aimed to establish whether chronic antidepressant treatment could alter the 
      modulation of the neurotrophin brain-derived neurotrophic factor (BDNF) under a 
      stressful condition. Therefore, adult male Sprague-Dawley rats were treated for 
      21 days with vehicle or with the SNRI duloxetine and, 24 h after the last 
      injection, exposed to an acute swim stress (5 min) before being killed 15 min 
      later. We found that chronic duloxetine treatment was able to modulate the rapid 
      transcriptional changes of BDNF isoforms produced by an acute swim stress. Indeed 
      whereas the mRNA levels of BDNF exon IV were upregulated by stress in vehicle as 
      well as in duloxetine-treated rats, a significant increase of exon VI and exon IX 
      was only found in rats that were pretreated with the antidepressant. These 
      differential effects are in part because of selective changes in signaling 
      pathways involved in the control of BDNF transcription. Moreover, the acute 
      stressful episode significantly increased the levels of mature BDNF protein in 
      the synaptosomal compartment in rats that were pretreated with the 
      antidepressant, but not in control animals. Our results suggest that chronic 
      antidepressant treatment might affect the responsiveness of BDNF under stressful 
      conditions, suggesting that pharmacological intervention could 'prime' 
      neuroprotective pathways and render them more responsive to preserve cell 
      function and viability.
FAU - Molteni, Raffaella
AU  - Molteni R
AD  - Center of Neuropharmacology, Department of Pharmacological Sciences, University 
      of Milan, Milan 20133, Italy.
FAU - Calabrese, Francesca
AU  - Calabrese F
FAU - Cattaneo, Annamaria
AU  - Cattaneo A
FAU - Mancini, Michele
AU  - Mancini M
FAU - Gennarelli, Massimo
AU  - Gennarelli M
FAU - Racagni, Giorgio
AU  - Racagni G
FAU - Riva, Marco A
AU  - Riva MA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20081119
PL  - England
TA  - Neuropsychopharmacology
JT  - Neuropsychopharmacology : official publication of the American College of 
      Neuropsychopharmacology
JID - 8904907
RN  - 0 (Antidepressive Agents)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Protein Isoforms)
RN  - 0 (RNA, Messenger)
RN  - 0 (Thiophenes)
RN  - 9044SC542W (Duloxetine Hydrochloride)
RN  - W980KJ009P (Corticosterone)
SB  - IM
EIN - Neuropsychopharmacology. 2009 Aug;34(9):2196
MH  - Animals
MH  - Antidepressive Agents/*therapeutic use
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Corticosterone/blood
MH  - Cytoplasm/drug effects/metabolism
MH  - Duloxetine Hydrochloride
MH  - Hippocampus/*drug effects/metabolism
MH  - Male
MH  - Protein Isoforms/metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Stress, Psychological/*drug therapy/physiopathology
MH  - Synaptosomes/drug effects/metabolism
MH  - Thiophenes/*therapeutic use
MH  - Transcription, Genetic/drug effects
MH  - Up-Regulation/drug effects
EDAT- 2008/11/21 09:00
MHDA- 2009/06/18 09:00
CRDT- 2008/11/21 09:00
PHST- 2008/11/21 09:00 [pubmed]
PHST- 2009/06/18 09:00 [medline]
PHST- 2008/11/21 09:00 [entrez]
AID - npp2008208 [pii]
AID - 10.1038/npp.2008.208 [doi]
PST - ppublish
SO  - Neuropsychopharmacology. 2009 May;34(6):1523-32. doi: 10.1038/npp.2008.208. Epub 
      2008 Nov 19.