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000137288 0247_ $$2doi$$a10.1093/jmcb/mjt046
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000137288 0247_ $$2ISSN$$a1673-520X
000137288 0247_ $$2ISSN$$a1674-2788
000137288 0247_ $$2ISSN$$a1759-4685
000137288 037__ $$aDZNE-2020-03610
000137288 041__ $$aEnglish
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000137288 1001_ $$0P:(DE-2719)2000028$$aWurst, Wolfgang$$b0$$eFirst author
000137288 245__ $$aWnt1-regulated genetic networks in midbrain dopaminergic neuron development.
000137288 260__ $$aOxford$$bOxford Univ. Press$$c2014
000137288 264_1 $$2Crossref$$3online$$bOxford University Press (OUP)$$c2013-12-09
000137288 264_1 $$2Crossref$$3print$$bOxford University Press (OUP)$$c2014-02-01
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000137288 520__ $$aNeurons synthesizing the neurotransmitter dopamine exert crucial functions in the mammalian brain. The biggest and most important population of dopamine-synthesizing neurons is located in the mammalian ventral midbrain (VM), and controls and modulates the execution of motor, cognitive, affective, motivational, and rewarding behaviours. Degeneration of these neurons leads to motor deficits that are characteristic of Parkinson's disease, while their dysfunction is involved in the pathogenesis of psychiatric disorders including schizophrenia and addiction. Because the aetiology and therapeutic prospects for these diseases include neurodevelopmental aspects, substantial scientific interest has been focused on deciphering the mechanistic pathways that control the generation and survival of these neurons during embryonic development. Researches during the last decade revealed the pivotal role of the secreted Wnt1 ligand and its signalling cascade in the generation of the dopamine-synthesizing neurons in the mammalian VM. Here, we summarize the initial and more recent findings that have unravelled several Wnt1-controlled genetic networks required for the proliferation and commitment of VM progenitors to the dopaminergic cell fate during midgestational embryonic stages, and for the correct differentiation of these progenitors into postmitotic dopamine-synthesizing neurons at late midgestational embryonic and foetal stages.
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000137288 650_7 $$2NLM Chemicals$$aWnt1 Protein
000137288 650_2 $$2MeSH$$aAnimals
000137288 650_2 $$2MeSH$$aDopaminergic Neurons: cytology
000137288 650_2 $$2MeSH$$aDopaminergic Neurons: metabolism
000137288 650_2 $$2MeSH$$aDopaminergic Neurons: physiology
000137288 650_2 $$2MeSH$$aGene Regulatory Networks
000137288 650_2 $$2MeSH$$aMesencephalon: cytology
000137288 650_2 $$2MeSH$$aMice
000137288 650_2 $$2MeSH$$aModels, Biological
000137288 650_2 $$2MeSH$$aWnt Signaling Pathway: physiology
000137288 650_2 $$2MeSH$$aWnt1 Protein: genetics
000137288 650_2 $$2MeSH$$aWnt1 Protein: metabolism
000137288 650_2 $$2MeSH$$aWnt1 Protein: physiology
000137288 7001_ $$0P:(DE-2719)9000256$$aPrakash, Nilima$$b1$$eLast author
000137288 77318 $$2Crossref$$3journal-article$$a10.1093/jmcb/mjt046$$b : Oxford University Press (OUP), 2013-12-09$$n1$$p34-41$$tJournal of Molecular Cell Biology$$v6$$x1674-2788$$y2013
000137288 773__ $$0PERI:(DE-600)2500949-7$$a10.1093/jmcb/mjt046$$gVol. 6, no. 1, p. 34 - 41$$n1$$p34-41$$q6:1<34 - 41$$tJournal of molecular cell biology$$v6$$x1674-2788$$y2013
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000137288 9131_ $$0G:(DE-HGF)POF3-342$$1G:(DE-HGF)POF3-340$$2G:(DE-HGF)POF3-300$$aDE-HGF$$bForschungsbereich Gesundheit$$lErkrankungen des Nervensystems$$vDisease Mechanisms and Model Systems$$x0
000137288 9141_ $$y2014
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