scholarly journals OTX2 Transcription Factor Controls Regional Patterning within the Medial Ganglionic Eminence and Regional Identity of the Septum

Cell Reports ◽  
2015 ◽  
Vol 12 (3) ◽  
pp. 482-494 ◽  
Author(s):  
Renée V. Hoch ◽  
Susan Lindtner ◽  
James D. Price ◽  
John L.R. Rubenstein
Keyword(s):  
Transcription Factor ◽  
Regional Identity ◽  
Medial Ganglionic Eminence ◽  
Ganglionic Eminence

scholarly journals Nf1deletion results in depletion of theLhx6transcription factor and a specific loss of parvalbumin+cortical interneurons

2020 ◽  
Vol 117 (11) ◽  
pp. 6189-6195 ◽  
Author(s):  
Kartik Angara ◽  
Emily Ling-Lin Pai ◽  
Stephanie M. Bilinovich ◽  
April M. Stafford ◽  
Julie T. Nguyen ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Mek Inhibitor ◽  
Gabaergic Interneurons ◽  
Medial Ganglionic Eminence ◽  
Ganglionic Eminence ◽  
Specific Loss ◽  
Developmental Milestone ◽  
Cortical Interneurons ◽  
Dose Dependent Decrease ◽  
Dose Dependent

Neurofibromatosis 1 (NF1) is caused by mutations in theNF1gene, which encodes the protein, neurofibromin, an inhibitor of Ras activity. Cortical GABAergic interneurons (CINs) are implicated in NF1 pathology, but the cellular and molecular changes to CINs are unknown. We deleted mouseNf1from the medial ganglionic eminence, which gives rise to both oligodendrocytes and CINs that express somatostatin and parvalbumin.Nf1loss led to a persistence of immature oligodendrocytes that prevented later-generated oligodendrocytes from occupying the cortex. Moreover, molecular and cellular properties of parvalbumin (PV)-positive CINs were altered by the loss ofNf1, without changes in somatostatin (SST)-positive CINs. We discovered that loss ofNf1results in a dose-dependent decrease inLhx6expression, the transcription factor necessary to establish SST+and PV+CINs, which was rescued by the MEK inhibitor SL327, revealing a mechanism whereby a neurofibromin/Ras/MEK pathway regulates a critical CIN developmental milestone.

scholarly journals Nf1 deletion results in depletion of the Lhx6 transcription factor and a specific loss of parvalbumin+ cortical interneurons

2019 ◽  
Author(s):  
Kartik Angara ◽  
Emily Ling-Lin Pai ◽  
Stephanie M Bilinovich ◽  
April M Stafford ◽  
Julie T Nguyen ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Benign Tumors ◽  
Gabaergic Interneurons ◽  
Medial Ganglionic Eminence ◽  
Ganglionic Eminence ◽  
Monogenic Disorder ◽  
Cognitive Changes ◽  
Specific Loss ◽  
Ras Gtpase ◽  
Cortical Interneurons

SummaryNeurofibromatosis-1 (NF-1) is a monogenic disorder caused by mutations in the NF1 gene, which encodes the protein, Neurofibromin, an inhibitor of Ras GTPase activity. While NF-1 is often characterized by café-au-lait skin spots and benign tumors, the mechanisms underlying cognitive changes in NF-1 are poorly understood. Cortical GABAergic interneurons (CINs) are implicated in NF-1 pathology but cellular and molecular changes to CINs are poorly understood. We deleted Nf1 from the medial ganglionic eminence (MGE), which gives rise to both oligodendrocytes and CINs that express somatostatin and parvalbumin. Loss of Nf1 led to a persistence of immature oligodendrocytes that prevented later born oligodendrocytes from occupying the cortex. Moreover, PV+ CINs were uniquely lost, without changes in SST+ CINs. We discovered that loss of Nf1 results in a graded decrease in Lhx6 expression, the transcription factor necessary to establish SST+ and PV+ CINs, revealing a mechanism whereby Nf1 regulates a critical CIN developmental milestone.

scholarly journals The Medial Ganglionic Eminence Gives Rise to a Population of Early Neurons in the Developing Cerebral Cortex

1999 ◽  
Vol 19 (18) ◽  
pp. 7881-7888 ◽  
Author(s):  
Alexandros A. Lavdas ◽  
Maria Grigoriou ◽  
Vassilis Pachnis ◽  
John G. Parnavelas
Keyword(s):  
Cerebral Cortex ◽  
Medial Ganglionic Eminence ◽  
Ganglionic Eminence

scholarly journals Generation and Fusion of Human Cortical and Medial Ganglionic Eminence Brain Organoids

2018 ◽  
Vol 47 (1) ◽  
pp. e61 ◽  
Author(s):  
Yangfei Xiang ◽  
Tanaka Yoshiaki ◽  
Benjamin Patterson ◽  
Bilal Cakir ◽  
Kun-Yong Kim ◽  
...  
Keyword(s):  
Medial Ganglionic Eminence ◽  
Ganglionic Eminence

Young neurons from medial ganglionic eminence disperse in adult and embryonic brain

10.1038/8131 ◽  
1999 ◽  
Vol 2 (5) ◽  
pp. 461-466 ◽  
Author(s):  
Hynek Wichterle ◽  
Jose Manuel Garcia-Verdugo ◽  
Daniel G. Herrera ◽  
Arturo Alvarez-Buylla
Keyword(s):  
Embryonic Brain ◽  
Medial Ganglionic Eminence ◽  
Ganglionic Eminence

scholarly journals Interneuron origins in the embryonic porcine medial ganglionic eminence

2020 ◽  
Author(s):  
Mariana L. Casalia ◽  
Tina Li ◽  
Harrison Ramsay ◽  
Pablo J. Ross ◽  
Mercedes F. Paredes ◽  
...  
Keyword(s):  
Expression Patterns ◽  
Normal Brain ◽  
Female Rat ◽  
Medial Ganglionic Eminence ◽  
Ganglionic Eminence ◽  
Embryonic Mouse ◽  
Migratory Capacity ◽  
Normal Brain Function ◽  
Transcription Factor Expression

Interneurons contribute to the complexity of neural circuits and maintenance of normal brain function. Rodent interneurons originate in embryonic ganglionic eminences, but developmental origins in other species are less understood. Here, we show that transcription factor expression patterns in porcine embryonic subpallium are similar to rodents, delineating a distinct medial ganglionic eminence (MGE) progenitor domain. On the basis of Nkx2.1, Lhx6 and Dlx2 expression, in vitro differentiation into neurons expressing GABA and robust migratory capacity in explant assays, we propose that cortical and hippocampal interneurons originate from a porcine MGE region. Following xenotransplantation into adult male and female rat hippocampus, we further demonstrate that porcine MGE progenitors, like those from rodents, migrate and differentiate into morphologically distinct interneurons expressing GABA. Our findings reveal that basic rules for interneuron development are conserved across species, and that porcine embryonic MGE progenitors could serve as a valuable source for interneuron-based xenotransplantation therapies.Significance StatementHere we demonstrate that porcine MGE, like rodents, exhibit a distinct transcriptional and pallial interneuron-specific antibody profile, in vitro migratory capacity and are amenable to xenotransplantation. This is the first comprehensive examination of embryonic pallial interneuron origins in the pig, and because a rich neurodevelopmental literature on embryonic mouse MGE exists (with some additional characterizations in other species like monkey and human) our work allows direct neurodevelopmental comparisons with this literature.

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