PMID- 26630005
OWN - NLM
STAT- MEDLINE
DCOM- 20160610
LR  - 20181113
IS  - 1091-6490 (Electronic)
IS  - 0027-8424 (Print)
IS  - 0027-8424 (Linking)
VI  - 112
IP  - 51
DP  - 2015 Dec 22
TI  - Neurotrophic-priming of glucocorticoid receptor signaling is essential for 
      neuronal plasticity to stress and antidepressant treatment.
PG  - 15737-42
LID - 10.1073/pnas.1509045112 [doi]
AB  - Neurotrophins and glucocorticoids are robust synaptic modifiers, and deregulation 
      of their activities is a risk factor for developing stress-related disorders. Low 
      levels of brain-derived neurotrophic factor (BDNF) increase the desensitization 
      of glucocorticoid receptors (GR) and vulnerability to stress, whereas higher 
      levels of BDNF facilitate GR-mediated signaling and the response to 
      antidepressants. However, the molecular mechanism underlying neurotrophic-priming 
      of GR function is poorly understood. Here we provide evidence that activation of 
      a TrkB-MAPK pathway, when paired with the deactivation of a GR-protein 
      phosphatase 5 pathway, resulted in sustained GR phosphorylation at BDNF-sensitive 
      sites that is essential for the transcription of neuronal plasticity genes. 
      Genetic strategies that disrupted GR phosphorylation or TrkB signaling in vivo 
      impaired the neuroplasticity to chronic stress and the effects of the 
      antidepressant fluoxetine. Our findings reveal that the coordinated actions of 
      BDNF and glucocorticoids promote neuronal plasticity and that disruption in 
      either pathway could set the stage for the development of stress-induced 
      psychiatric diseases.
FAU - Arango-Lievano, Margarita
AU  - Arango-Lievano M
AD  - Deptartment of Physiology, Institut de Genomique Fonctionnelle, INSERM U1191, 
      CNRS UMR5203, University of Montpellier, Montpellier 34070, France; 
      Margarita.arango@igf.cnrs.fr freddy.jeanneteau@igf.cnrs.fr.
FAU - Lambert, W Marcus
AU  - Lambert WM
AD  - Department of Microbiology, New York University Langone Medical Center, New York, 
      NY 10016;
FAU - Bath, Kevin G
AU  - Bath KG
AD  - Department of Cognitive, Linguistic, and Psychological Sciences, Brown 
      University, Providence, RI 02912;
FAU - Garabedian, Michael J
AU  - Garabedian MJ
AD  - Department of Microbiology, New York University Langone Medical Center, New York, 
      NY 10016;
FAU - Chao, Moses V
AU  - Chao MV
AD  - Department of Cell Biology, Physiology, and Neuroscience and Department of 
      Psychiatry, New York University Langone Medical Center, New York, NY 10016.
FAU - Jeanneteau, Freddy
AU  - Jeanneteau F
AD  - Deptartment of Physiology, Institut de Genomique Fonctionnelle, INSERM U1191, 
      CNRS UMR5203, University of Montpellier, Montpellier 34070, France; 
      Margarita.arango@igf.cnrs.fr freddy.jeanneteau@igf.cnrs.fr.
LA  - eng
GR  - R01 MH086651/MH/NIMH NIH HHS/United States
GR  - MH086651/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20151116
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 0 (Antidepressive Agents)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Receptors, Glucocorticoid)
RN  - 01K63SUP8D (Fluoxetine)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 2.7.10.1 (tropomyosin-related kinase-B, human)
SB  - IM
CIN - Proc Natl Acad Sci U S A. 2015 Dec 22;112(51):15544-5. PMID: 26627713
MH  - Animals
MH  - Antidepressive Agents/*pharmacology
MH  - Brain-Derived Neurotrophic Factor/physiology
MH  - Female
MH  - Fluoxetine/pharmacology
MH  - MAP Kinase Signaling System
MH  - Membrane Glycoproteins/physiology
MH  - Mice
MH  - Neuronal Plasticity/drug effects/*physiology
MH  - Phosphorylation
MH  - Protein-Tyrosine Kinases/physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB
MH  - Receptors, Glucocorticoid/*physiology
MH  - Signal Transduction/*physiology
MH  - Stress, Psychological/*physiopathology
PMC - PMC4697403
OTO - NOTNLM
OT  - BDNF
OT  - antidepressant
OT  - coincidence detection
OT  - glucocorticoid
OT  - stress
COIS- The authors declare no conflict of interest.
EDAT- 2015/12/03 06:00
MHDA- 2016/06/11 06:00
PMCR- 2015/11/16
CRDT- 2015/12/03 06:00
PHST- 2015/12/03 06:00 [entrez]
PHST- 2015/12/03 06:00 [pubmed]
PHST- 2016/06/11 06:00 [medline]
PHST- 2015/11/16 00:00 [pmc-release]
AID - 1509045112 [pii]
AID - 201509045 [pii]
AID - 10.1073/pnas.1509045112 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 2015 Dec 22;112(51):15737-42. doi: 
      10.1073/pnas.1509045112. Epub 2015 Nov 16.