Transgenic mice lacking CREB and CREM in noradrenergic and serotonergic neurons respond differently to common antidepressants on tail suspension test

Abstract Evidence exists that chronic antidepressant therapy enhances CREB levels and activity. Nevertheless, the data are not conclusive, as previous analysis of transgenic mouse models has suggested that CREB inactivation in fact contributes to antidepressant-like behavior. The aim of this study w...

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Autores principales:	Katarzyna Rafa–Zabłocka, Grzegorz Kreiner, Monika Bagińska, Justyna Kuśmierczyk, Rosanna Parlato, Irena Nalepa
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/a1b7e3eb2dd2473daa4f073cdd043deb
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spelling	oai:doaj.org-article:a1b7e3eb2dd2473daa4f073cdd043deb2021-12-02T15:05:17ZTransgenic mice lacking CREB and CREM in noradrenergic and serotonergic neurons respond differently to common antidepressants on tail suspension test10.1038/s41598-017-14069-62045-2322https://doaj.org/article/a1b7e3eb2dd2473daa4f073cdd043deb2017-10-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-14069-6https://doaj.org/toc/2045-2322Abstract Evidence exists that chronic antidepressant therapy enhances CREB levels and activity. Nevertheless, the data are not conclusive, as previous analysis of transgenic mouse models has suggested that CREB inactivation in fact contributes to antidepressant-like behavior. The aim of this study was to evaluate the role of CREB in this context by exploiting novel transgenic mouse models, characterized by selective ablation of CREB restricted to noradrenergic (Creb1DBHCre/Crem−/−) or serotonergic (Creb1TPH2CreERT2/Crem−/−) neurons in a CREM-deficient background to avoid possible compensatory effects of CREM. Selective and functional ablation of CREB affected antidepressant-like behavior in a tail suspension test (TST) after antidepressant treatment. Contrary to single Creb1DBHCre mutants, Creb1DBHCre/Crem−/− mice did not respond to acute desipramine administration (20 mg/kg) on the TST. On the other hand, single Creb1TPH2CreERT2 mutants displayed reduced responses to fluoxetine (10 mg/kg) on the TST, while the effects in Creb1TPH2CreERT2/Crem−/− mice differed by gender. Our results provide further evidence for the important role of CREM as a compensatory factor. Additionally, the results indicate that new models based on the functional ablation of CREB in select neuronal populations may represent a valuable tool for investigating the role of CREB in the mechanism of antidepressant therapy.Katarzyna Rafa–ZabłockaGrzegorz KreinerMonika BagińskaJustyna KuśmierczykRosanna ParlatoIrena NalepaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Katarzyna Rafa–Zabłocka Grzegorz Kreiner Monika Bagińska Justyna Kuśmierczyk Rosanna Parlato Irena Nalepa Transgenic mice lacking CREB and CREM in noradrenergic and serotonergic neurons respond differently to common antidepressants on tail suspension test
description	Abstract Evidence exists that chronic antidepressant therapy enhances CREB levels and activity. Nevertheless, the data are not conclusive, as previous analysis of transgenic mouse models has suggested that CREB inactivation in fact contributes to antidepressant-like behavior. The aim of this study was to evaluate the role of CREB in this context by exploiting novel transgenic mouse models, characterized by selective ablation of CREB restricted to noradrenergic (Creb1DBHCre/Crem−/−) or serotonergic (Creb1TPH2CreERT2/Crem−/−) neurons in a CREM-deficient background to avoid possible compensatory effects of CREM. Selective and functional ablation of CREB affected antidepressant-like behavior in a tail suspension test (TST) after antidepressant treatment. Contrary to single Creb1DBHCre mutants, Creb1DBHCre/Crem−/− mice did not respond to acute desipramine administration (20 mg/kg) on the TST. On the other hand, single Creb1TPH2CreERT2 mutants displayed reduced responses to fluoxetine (10 mg/kg) on the TST, while the effects in Creb1TPH2CreERT2/Crem−/− mice differed by gender. Our results provide further evidence for the important role of CREM as a compensatory factor. Additionally, the results indicate that new models based on the functional ablation of CREB in select neuronal populations may represent a valuable tool for investigating the role of CREB in the mechanism of antidepressant therapy.
format	article
author	Katarzyna Rafa–Zabłocka Grzegorz Kreiner Monika Bagińska Justyna Kuśmierczyk Rosanna Parlato Irena Nalepa
author_facet	Katarzyna Rafa–Zabłocka Grzegorz Kreiner Monika Bagińska Justyna Kuśmierczyk Rosanna Parlato Irena Nalepa
author_sort	Katarzyna Rafa–Zabłocka
title	Transgenic mice lacking CREB and CREM in noradrenergic and serotonergic neurons respond differently to common antidepressants on tail suspension test
title_short	Transgenic mice lacking CREB and CREM in noradrenergic and serotonergic neurons respond differently to common antidepressants on tail suspension test
title_full	Transgenic mice lacking CREB and CREM in noradrenergic and serotonergic neurons respond differently to common antidepressants on tail suspension test
title_fullStr	Transgenic mice lacking CREB and CREM in noradrenergic and serotonergic neurons respond differently to common antidepressants on tail suspension test
title_full_unstemmed	Transgenic mice lacking CREB and CREM in noradrenergic and serotonergic neurons respond differently to common antidepressants on tail suspension test
title_sort	transgenic mice lacking creb and crem in noradrenergic and serotonergic neurons respond differently to common antidepressants on tail suspension test
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/a1b7e3eb2dd2473daa4f073cdd043deb
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Transgenic mice lacking CREB and CREM in noradrenergic and serotonergic neurons respond differently to common antidepressants on tail suspension test

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