PMID- 30214393
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 1662-5099 (Print)
IS  - 1662-5099 (Electronic)
IS  - 1662-5099 (Linking)
VI  - 11
DP  - 2018
TI  - cAMP Response Element-Binding Protein (CREB): A Possible Signaling Molecule Link 
      in the Pathophysiology of Schizophrenia.
PG  - 255
LID - 10.3389/fnmol.2018.00255 [doi]
LID - 255
AB  - Dopamine is a brain neurotransmitter involved in the pathology of schizophrenia. 
      The dopamine hypothesis states that, in schizophrenia, dopaminergic signal 
      transduction is hyperactive. The cAMP-response element binding protein (CREB) is 
      an intracellular protein that regulates the expression of genes that are 
      important in dopaminergic neurons. Dopamine affects the phosphorylation of CREB 
      via G protein-coupled receptors. Neurotrophins, such as brain derived growth 
      factor (BDNF), are critical regulators during neurodevelopment and synaptic 
      plasticity. The CREB is one of the major regulators of neurotrophin responses 
      since phosphorylated CREB binds to a specific sequence in the promoter of BDNF 
      and regulates its transcription. Moreover, susceptibility genes associated with 
      schizophrenia also target and stimulate the activity of CREB. Abnormalities of 
      CREB expression is observed in the brain of individuals suffering from 
      schizophrenia, and two variants (-933T to C and -413G to A) were found only in 
      schizophrenic patients. The CREB was also involved in the therapy of animal 
      models of schizophrenia. Collectively, these findings suggest a link between CREB 
      and the pathophysiology of schizophrenia. This review provides an overview of 
      CREB structure, expression, and biological functions in the brain and its 
      interaction with dopamine signaling, neurotrophins, and susceptibility genes for 
      schizophrenia. Animal models in which CREB function is modulated, by either 
      overexpression of the protein or knocked down through gene deletion/mutation, 
      implicating CREB in schizophrenia and antipsychotic drugs efficacy are also 
      discussed. Targeting research and drug development on CREB could potentially 
      accelerate the development of novel medications against schizophrenia.
FAU - Wang, Haitao
AU  - Wang H
AD  - Department of Neuropharmacology and Drug Discovery, School of Pharmaceutical 
      Sciences, Southern Medical University, Guangzhou, China.
FAU - Xu, Jiangping
AU  - Xu J
AD  - Department of Neuropharmacology and Drug Discovery, School of Pharmaceutical 
      Sciences, Southern Medical University, Guangzhou, China.
FAU - Lazarovici, Philip
AU  - Lazarovici P
AD  - School of Pharmacy Institute for Drug Research, Faculty of Medicine, The Hebrew 
      University of Jerusalem, Jerusalem, Israel.
FAU - Quirion, Remi
AU  - Quirion R
AD  - Douglas Mental Health University Institute, McGill University, Montreal, QC, 
      Canada.
FAU - Zheng, Wenhua
AU  - Zheng W
AD  - Faculty of Health Sciences, University of Macau, Taipa, China.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20180830
PL  - Switzerland
TA  - Front Mol Neurosci
JT  - Frontiers in molecular neuroscience
JID - 101477914
PMC - PMC6125665
OTO - NOTNLM
OT  - CREB
OT  - dopamine
OT  - neurodevelopment
OT  - neurotransmitter
OT  - schizophrenia
EDAT- 2018/09/15 06:00
MHDA- 2018/09/15 06:01
PMCR- 2018/01/01
CRDT- 2018/09/15 06:00
PHST- 2018/04/03 00:00 [received]
PHST- 2018/07/06 00:00 [accepted]
PHST- 2018/09/15 06:00 [entrez]
PHST- 2018/09/15 06:00 [pubmed]
PHST- 2018/09/15 06:01 [medline]
PHST- 2018/01/01 00:00 [pmc-release]
AID - 10.3389/fnmol.2018.00255 [doi]
PST - epublish
SO  - Front Mol Neurosci. 2018 Aug 30;11:255. doi: 10.3389/fnmol.2018.00255. 
      eCollection 2018.