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Abnormal retinoid and TrkB signaling in the prefrontal cortex in mood disorders. / Qi, Xin-Rui; Zhao, Juan; Liu, Ji; Fang, Hui; Swaab, Dick F; Zhou, Jiang-Ning.

In: Cerebral Cortex, Vol. 25, No. 1, 01.2015, p. 75-83.

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Qi, Xin-Rui ; Zhao, Juan ; Liu, Ji ; Fang, Hui ; Swaab, Dick F ; Zhou, Jiang-Ning. / Abnormal retinoid and TrkB signaling in the prefrontal cortex in mood disorders. In: Cerebral Cortex. 2015 ; Vol. 25, No. 1. pp. 75-83.

BibTeX

@article{d76275f3da1e4e9a91e9ec8877c44263,
title = "Abnormal retinoid and TrkB signaling in the prefrontal cortex in mood disorders",
abstract = "The prefrontal cortex shows structural and functional alterations in mood disorders. Retinoid signaling, brain-derived neurotrophic factor (BDNF), and its receptor TrkB are reported to be involved in depression. Here, we found that mRNA levels of key elements of retinoid signaling were significantly reduced in the postmortem dorsolateral prefrontal cortex/anterior cingulate cortex (ACC) from elderly depressed patients who did not die from suicide. Decreased mRNA levels of BDNF and TrkB isoforms were also found. Similar alterations were observed in rats subjected to chronic unpredictable mild stress. Along with neurons immunopositive for both retinoic acid receptor-α (RARα) and TrkB, a positive correlation between mRNA levels of the 2 receptors was found in the ACC of control subjects but not of depressed patients. In vitro studies showed that RARα was able to bind to and transactivate the TrkB promoter via a putative RA response element within the TrkB promoter. In conclusion, the retinoid and BDNF-TrkB signaling in the prefrontal cortex are compromised in mood disorders, and the transcriptional upregulation of TrkB by RARα provide a possible mechanism for their interaction. The retinoid signaling pathway that may activate TrkB expression will be an alternative novel target for BDNF-based antidepressant treatment.",
keywords = "Aged, Aldehyde Dehydrogenase, Aldehyde Oxidoreductases, Animals, Bipolar Disorder, Brain-Derived Neurotrophic Factor, CHO Cells, Cell Line, Tumor, Cricetulus, Depressive Disorder, Major, Female, Gyrus Cinguli, Humans, Male, Membrane Glycoproteins, Neuroblastoma, Neurons, Prefrontal Cortex, Protein-Tyrosine Kinases, RNA, Messenger, Rats, Rats, Sprague-Dawley, Retinoid X Receptor alpha, Retinoid X Receptor beta, Retinoid X Receptors, Signal Transduction, Stress, Psychological",
author = "Xin-Rui Qi and Juan Zhao and Ji Liu and Hui Fang and Swaab, {Dick F} and Jiang-Ning Zhou",
note = "{\circledC} The Author 2013. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.",
year = "2015",
month = "1",
doi = "10.1093/cercor/bht203",
language = "English",
volume = "25",
pages = "75--83",
journal = "Cerebral Cortex",
issn = "1047-3211",
publisher = "Oxford University Press",
number = "1",

}

RIS

TY - JOUR

T1 - Abnormal retinoid and TrkB signaling in the prefrontal cortex in mood disorders

AU - Qi, Xin-Rui

AU - Zhao, Juan

AU - Liu, Ji

AU - Fang, Hui

AU - Swaab, Dick F

AU - Zhou, Jiang-Ning

N1 - © The Author 2013. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

PY - 2015/1

Y1 - 2015/1

N2 - The prefrontal cortex shows structural and functional alterations in mood disorders. Retinoid signaling, brain-derived neurotrophic factor (BDNF), and its receptor TrkB are reported to be involved in depression. Here, we found that mRNA levels of key elements of retinoid signaling were significantly reduced in the postmortem dorsolateral prefrontal cortex/anterior cingulate cortex (ACC) from elderly depressed patients who did not die from suicide. Decreased mRNA levels of BDNF and TrkB isoforms were also found. Similar alterations were observed in rats subjected to chronic unpredictable mild stress. Along with neurons immunopositive for both retinoic acid receptor-α (RARα) and TrkB, a positive correlation between mRNA levels of the 2 receptors was found in the ACC of control subjects but not of depressed patients. In vitro studies showed that RARα was able to bind to and transactivate the TrkB promoter via a putative RA response element within the TrkB promoter. In conclusion, the retinoid and BDNF-TrkB signaling in the prefrontal cortex are compromised in mood disorders, and the transcriptional upregulation of TrkB by RARα provide a possible mechanism for their interaction. The retinoid signaling pathway that may activate TrkB expression will be an alternative novel target for BDNF-based antidepressant treatment.

AB - The prefrontal cortex shows structural and functional alterations in mood disorders. Retinoid signaling, brain-derived neurotrophic factor (BDNF), and its receptor TrkB are reported to be involved in depression. Here, we found that mRNA levels of key elements of retinoid signaling were significantly reduced in the postmortem dorsolateral prefrontal cortex/anterior cingulate cortex (ACC) from elderly depressed patients who did not die from suicide. Decreased mRNA levels of BDNF and TrkB isoforms were also found. Similar alterations were observed in rats subjected to chronic unpredictable mild stress. Along with neurons immunopositive for both retinoic acid receptor-α (RARα) and TrkB, a positive correlation between mRNA levels of the 2 receptors was found in the ACC of control subjects but not of depressed patients. In vitro studies showed that RARα was able to bind to and transactivate the TrkB promoter via a putative RA response element within the TrkB promoter. In conclusion, the retinoid and BDNF-TrkB signaling in the prefrontal cortex are compromised in mood disorders, and the transcriptional upregulation of TrkB by RARα provide a possible mechanism for their interaction. The retinoid signaling pathway that may activate TrkB expression will be an alternative novel target for BDNF-based antidepressant treatment.

KW - Aged

KW - Aldehyde Dehydrogenase

KW - Aldehyde Oxidoreductases

KW - Animals

KW - Bipolar Disorder

KW - Brain-Derived Neurotrophic Factor

KW - CHO Cells

KW - Cell Line, Tumor

KW - Cricetulus

KW - Depressive Disorder, Major

KW - Female

KW - Gyrus Cinguli

KW - Humans

KW - Male

KW - Membrane Glycoproteins

KW - Neuroblastoma

KW - Neurons

KW - Prefrontal Cortex

KW - Protein-Tyrosine Kinases

KW - RNA, Messenger

KW - Rats

KW - Rats, Sprague-Dawley

KW - Retinoid X Receptor alpha

KW - Retinoid X Receptor beta

KW - Retinoid X Receptors

KW - Signal Transduction

KW - Stress, Psychological

U2 - 10.1093/cercor/bht203

DO - 10.1093/cercor/bht203

M3 - Article

VL - 25

SP - 75

EP - 83

JO - Cerebral Cortex

JF - Cerebral Cortex

SN - 1047-3211

IS - 1

ER -

ID: 2203175