PMID- 24946016
OWN - NLM
STAT- MEDLINE
DCOM- 20150526
LR  - 20211021
IS  - 1469-5111 (Electronic)
IS  - 1461-1457 (Print)
IS  - 1461-1457 (Linking)
VI  - 17
IP  - 11
DP  - 2014 Nov
TI  - Stress-induced alterations in 5-HT1A receptor transcriptional modulators NUDR and 
      Freud-1.
PG  - 1763-75
LID - 10.1017/S146114571400100X [doi]
AB  - The effect of stress on the mRNA and protein level of the 5-HT1A receptor and two 
      of its key transcriptional modulators, NUDR and Freud-1, was examined in the 
      prefrontal cortex (PFC) and hippocampus (Hp) using rodent models: olfactory 
      bulbectomy (OB) and prenatal stress (PS) in male and female rats; chronic mild 
      stress in male rats (CMS) and pregnancy stress. In PFC, CMS induced the most 
      widespread changes, with significant reduction in both mRNA and protein levels of 
      NUDR, 5-HT1A receptor and in Freud-1 mRNA; while in Hp 5-HT1A receptor and 
      Freud-1 protein levels were also decreased. In male, but not female OB rats PFC 
      Freud-1 and 5-HT1A receptor protein levels were reduced, while in Hp 5-HT1A 
      receptor, Freud-1 and NUDR mRNA's but not protein were reduced. In PS rats PFC 
      5-HT1A receptor protein was reduced more in females than males; while in Hp 
      Freud-1 protein was increased in females. In pregnancy stress, PFC NUDR, Freud-1 
      and 5-HT1A protein receptor levels were reduced, and in HP 5-HT1A receptor 
      protein levels were also reduced; in HP only NUDR and Freud-1 mRNA levels were 
      reduced. Overall, CMS and stress during pregnancy produced the most salient 
      changes in 5-HT1A receptor and transcription factor expression, suggesting a 
      primary role for altered transcription factor expression in chronic regulation of 
      5-HT1A receptor expression. By contrast, OB (in males) and PS (in females) 
      produced gender-specific reductions in PFC 5-HT1A receptor protein levels, 
      suggesting a role for post-transcriptional regulation. These and previous data 
      suggest that chronic stress might be a key regulator of NUDR/Freud-1 gene 
      expression.
FAU - Szewczyk, Bernadeta
AU  - Szewczyk B
AD  - Department of Neurobiology,Institute of Pharmacology, Polish Academy of 
      Sciences,Smetna 12, 31-343 Krakow,Poland.
FAU - Kotarska, Katarzyna
AU  - Kotarska K
AD  - Department of Neurobiology,Institute of Pharmacology, Polish Academy of 
      Sciences,Smetna 12, 31-343 Krakow,Poland.
FAU - Daigle, Mireille
AU  - Daigle M
AD  - Ottawa Hospital Research Institute (Neuroscience), University of Ottawa,451 Smyth 
      Road, Ottawa, ON,Canada.
FAU - Misztak, Paulina
AU  - Misztak P
AD  - Department of Neurobiology,Institute of Pharmacology, Polish Academy of 
      Sciences,Smetna 12, 31-343 Krakow,Poland.
FAU - Sowa-Kucma, Magdalena
AU  - Sowa-Kucma M
AD  - Department of Neurobiology,Institute of Pharmacology, Polish Academy of 
      Sciences,Smetna 12, 31-343 Krakow,Poland.
FAU - Rafalo, Anna
AU  - Rafalo A
AD  - Department of Neurobiology,Institute of Pharmacology, Polish Academy of 
      Sciences,Smetna 12, 31-343 Krakow,Poland.
FAU - Curzytek, Katarzyna
AU  - Curzytek K
AD  - Department of Experimental Neuroendocrinology,Institute of Pharmacology, Polish 
      Academy of Sciences,Smetna 12, PL 31-343 Krakow,Poland.
FAU - Kubera, Marta
AU  - Kubera M
AD  - Department of Experimental Neuroendocrinology,Institute of Pharmacology, Polish 
      Academy of Sciences,Smetna 12, PL 31-343 Krakow,Poland.
FAU - Basta-Kaim, Agnieszka
AU  - Basta-Kaim A
AD  - Department of Experimental Neuroendocrinology,Institute of Pharmacology, Polish 
      Academy of Sciences,Smetna 12, PL 31-343 Krakow,Poland.
FAU - Nowak, Gabriel
AU  - Nowak G
AD  - Department of Neurobiology,Institute of Pharmacology, Polish Academy of 
      Sciences,Smetna 12, 31-343 Krakow,Poland.
FAU - Albert, Paul R
AU  - Albert PR
AD  - Ottawa Hospital Research Institute (Neuroscience), University of Ottawa,451 Smyth 
      Road, Ottawa, ON,Canada.
LA  - eng
GR  - 115098-1/Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140619
PL  - England
TA  - Int J Neuropsychopharmacol
JT  - The international journal of neuropsychopharmacology
JID - 9815893
RN  - 0 (Cc2d1a protein, rat)
RN  - 0 (Deaf1 protein, rat)
RN  - 0 (Nuclear Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Repressor Proteins)
RN  - 0 (Transcription Factors)
RN  - 112692-38-3 (Receptor, Serotonin, 5-HT1A)
SB  - IM
MH  - Animals
MH  - Brain/*metabolism
MH  - Disease Models, Animal
MH  - Female
MH  - Gene Expression Regulation/*physiology
MH  - Male
MH  - Nuclear Proteins/genetics/*metabolism
MH  - Olfactory Bulb/surgery
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/physiopathology
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Receptor, Serotonin, 5-HT1A/genetics/*metabolism
MH  - Repressor Proteins/genetics/*metabolism
MH  - Sex Factors
MH  - Stress, Psychological/etiology/*pathology
MH  - Transcription Factors
PMC - PMC4514527
MID - CAMS4920
OID - NLM: CAMS4920
EDAT- 2014/06/20 06:00
MHDA- 2015/05/27 06:00
PMCR- 2015/07/24
CRDT- 2014/06/20 06:00
PHST- 2014/06/20 06:00 [entrez]
PHST- 2014/06/20 06:00 [pubmed]
PHST- 2015/05/27 06:00 [medline]
PHST- 2015/07/24 00:00 [pmc-release]
AID - S146114571400100X [pii]
AID - 10.1017/S146114571400100X [doi]
PST - ppublish
SO  - Int J Neuropsychopharmacol. 2014 Nov;17(11):1763-75. doi: 
      10.1017/S146114571400100X. Epub 2014 Jun 19.