PMID- 21254899
OWN - NLM
STAT- MEDLINE
DCOM- 20111011
LR  - 20131121
IS  - 1365-2060 (Electronic)
IS  - 0785-3890 (Linking)
VI  - 43
IP  - 5
DP  - 2011 Aug
TI  - A role for glucocorticoid-signaling in depression-like behavior of 
      gastrin-releasing peptide receptor knock-out mice.
PG  - 389-402
LID - 10.3109/07853890.2010.538716 [doi]
AB  - Abstract Background. The gastrin-releasing peptide receptor (GRPR) is highly 
      expressed in the limbic system, where it importantly regulates emotional 
      functions and in the suprachiasmatic nucleus, where it is central for the photic 
      resetting of the circadian clock. Mice lacking GRPR presented with deficient 
      light-induced phase shift in activity as well altered emotional learning and 
      amygdala function. The effect of GRPR deletion on depression-like behavior and 
      its molecular signature in the amygdala, however, has not yet been evaluated. 
      Methods. GRPR knock-out mice (GRPR-KO) were tested in the forced-swim test and 
      the sucrose preference test for depression-like behavior. Gene expression in the 
      basolateral nucleus of the amygdala was evaluated by micorarray analysis 
      subsequent to laser-capture microdissection-assisted extraction of mRNA. The 
      expression of selected genes was confirmed by RT-PCR. Results. GRPR-KO mice were 
      found to present with increased depression-like behavior. Microarray analysis 
      revealed down-regulation of several glucocorticoid-responsive genes in the 
      basolateral amygdala. Acute administration of dexamethasone reversed the 
      behavioral phenotype and alterations in gene expression. Discussion. We propose 
      that deletion of GRPR leads to the induction of depression-like behavior which is 
      paralleled by dysregulation of amygdala gene expression, potentially resulting 
      from deficient light-induced corticosterone release in GRPR-KO.
FAU - Monje, Francisco J
AU  - Monje FJ
AD  - Department of Physiology, Center for Physiology and Pharmacology, Medical 
      University of Vienna , Austria.
FAU - Kim, Eun-Jung
AU  - Kim EJ
FAU - Cabatic, Maureen
AU  - Cabatic M
FAU - Lubec, Gert
AU  - Lubec G
FAU - Herkner, Kurt R
AU  - Herkner KR
FAU - Pollak, Daniela D
AU  - Pollak DD
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110124
PL  - England
TA  - Ann Med
JT  - Annals of medicine
JID - 8906388
RN  - 0 (Glucocorticoids)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Bombesin)
RN  - 7S5I7G3JQL (Dexamethasone)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Amygdala/metabolism
MH  - Animals
MH  - Behavior, Animal/*drug effects
MH  - Corticosterone/metabolism
MH  - Depression/*physiopathology
MH  - Dexamethasone/*pharmacology
MH  - Disease Models, Animal
MH  - Down-Regulation
MH  - Gene Deletion
MH  - Gene Expression Regulation/drug effects
MH  - Glucocorticoids/pharmacology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Microarray Analysis
MH  - RNA, Messenger/metabolism
MH  - Receptors, Bombesin/*genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2011/01/25 06:00
MHDA- 2011/10/12 06:00
CRDT- 2011/01/25 06:00
PHST- 2011/01/25 06:00 [entrez]
PHST- 2011/01/25 06:00 [pubmed]
PHST- 2011/10/12 06:00 [medline]
AID - 10.3109/07853890.2010.538716 [doi]
PST - ppublish
SO  - Ann Med. 2011 Aug;43(5):389-402. doi: 10.3109/07853890.2010.538716. Epub 2011 Jan 
      24.