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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004902naa a2200505 4500
001oai:DiVA.org:oru-83056
003SwePub
008200612s2018 | |||||||||||000 ||eng|
009oai:DiVA.org:su-161025
009oai:prod.swepub.kib.ki.se:139236444
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-830562 URI
0247 a https://doi.org/10.1124/mol.118.1123422 DOI
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-1610252 URI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:1392364442 URI
040 a (SwePub)orud (SwePub)sud (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Lupu, Dianau Department of Toxicology, Iuliu Haţieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania; Unit Toxicol Sci, Karolinska Institute, Södertälje, Sweden4 aut
2451 0a Fluoxetine Affects Differentiation of Midbrain Dopaminergic Neurons In Vitro
264 c 2018-08-16
264 1a New York :b American Society for Pharmacology and Experimental Therapeutics,c 2018
338 a print2 rdacarrier
500 a Ytterligare forskningsfinansiär: Emil and Wera Cornell's research foundation
520 a Recent meta-analyses found an association between prenatal exposure to the antidepressant fluoxetine (FLX) and an increased risk of autism in children. This developmental disorder has been related to dysfunctions in the brains' rewards circuitry, which, in turn, has been linked to dysfunctions in dopaminergic (DA) signaling. The present study investigated if FLX affects processes involved in dopaminergic neuronal differentiation. Mouse neuronal precursors were differentiated into midbrain dopaminergic precursor cells (mDPCs) and concomitantly exposed to clinically relevant doses of FLX. Subsequently, dopaminergic precursors were evaluated for expression of differentiation and stemness markers using quantitative polymerase chain reaction. FLX treatment led to increases in early regional specification markers orthodenticle homeobox 2 (Otx2) and homeobox engrailed-1 and -2 (En1 and En2). On the other hand, two transcription factors essential for midbrain dopaminergic (mDA) neurogenesis, LIM homeobox transcription factor 1 alpha (Lmx1a) and paired-like homeodomain transcription factor 3 (Pitx3) were downregulated by FLX treatment. The stemness marker nestin (Nes) was increased, whereas the neuronal differentiation marker beta 3-tubulin (Tubb3) decreased. Additionally, we observed that FLX modulates the expression of several genes associated with autism spectrum disorder and downregulates the estrogen receptors (ERs) alpha and beta. Further investigations using ER beta knockout (BERKO) mDPCs showed that FLX had no or even opposite effects on several of the genes analyzed. These findings suggest that FLX affects differentiation of the dopaminergic system by increasing production of dopaminergic precursors, yet decreasing their maturation, partly via interference with the estrogen system.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
650 7a NATURVETENSKAPx Data- och informationsvetenskap0 (SwePub)1022 hsv//swe
650 7a NATURAL SCIENCESx Computer and Information Sciences0 (SwePub)1022 hsv//eng
7001 a Varshney, Mukesh K.u Karolinska Institutet4 aut
7001 a Mucs, Danielu Karolinska Institutet4 aut
7001 a Inzunza, Joseu Karolinska Institutet4 aut
7001 a Norinder, Ulf,d 1956-u Stockholms universitet,Institutionen för data- och systemvetenskap,Swetox, Karolinska Institutet, Sweden4 aut0 (Swepub:su)unori
7001 a Loghin, Feliciau Department of Toxicology, Iuliu Haţieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania4 aut
7001 a Nalvarte, Ivanu Karolinska Institutet4 aut
7001 a Ruegg, Joelleu Karolinska Institutet4 aut
7102 a Karolinska Institutetb Department of Toxicology, Iuliu Haţieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania; Unit Toxicol Sci, Karolinska Institute, Södertälje, Sweden4 org
7730 t Molecular Pharmacologyd New York : American Society for Pharmacology and Experimental Therapeuticsg 94:4, s. 1220-1231q 94:4<1220-1231x 0026-895Xx 1521-0111
8564 u https://doi.org/10.1124/mol.118.112342y Fulltext
8564 u https://molpharm.aspetjournals.org/content/molpharm/94/4/1220.full.pdf
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-83056
8564 8u https://doi.org/10.1124/mol.118.112342
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-161025
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:139236444

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