ArticleProceedings of the National Academy of Sciences of the United States of America2020
Parcellation of the striatal complex into dorsal and ventral districts.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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25 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Pooled it
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- Article
- CHL1 depletion affects dopamine receptor D2-dependent modulation of mouse behavior.Frontiers in behavioral neuroscience · 2023Article
- The brain of the tree pangolin (Manis tricuspis). VIII. The subpallial telencephalon.The Journal of comparative neurology · 2022Article
- Transcription factor Sp9 is a negative regulator of D1-type MSN development.Cell death discovery · 2022Article
- Dlx1/2-dependent expression of Meis2 promotes neuronal fate determination in the mammalian striatum.Development (Cambridge, England) · 2022Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The striatal complex of basal ganglia comprises two functionally distinct districts. The dorsal district controls motor and cognitive functions. The ventral district regulates the limbic function of motivation, reward, and emotion. The dorsoventral parcellation of the striatum also is of clinical importance as differential striatal pathophysiologies occur in Huntington's disease, Parkinson's disease, and drug addiction disorders. Despite these striking neurobiologic contrasts, it is largely unknown how the dorsal and ventral divisions of the striatum are set up. Here, we demonstrate that interactions between the two key transcription factors Nolz-1 and Dlx1/2 control the migratory paths of striatal neurons to the dorsal or ventral striatum. Moreover, these same transcription factors control the cell identity of striatal projection neurons in both the dorsal and the ventral striata including the D1-direct and D2-indirect pathways. We show that Nolz-1, through the I12b enhancer, represses
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