scholarly journals JNK signaling is required for proper tangential migration and laminar allocation of cortical interneurons

Development ◽  
2020 ◽  
Vol 147 (2) ◽  
pp. dev180646 ◽  
Author(s):  
Abigail K. Myers ◽  
Jessica G. Cunningham ◽  
Skye E. Smith ◽  
John P. Snow ◽  
Catherine A. Smoot ◽  
...  
Keyword(s):  
Jnk Signaling ◽  
Tangential Migration ◽  
Cortical Interneurons

scholarly journals Meningeal defects alter the tangential migration of cortical interneurons in Foxc1hith/hith mice

2012 ◽  
Vol 7 (1) ◽  
pp. 2 ◽  
Author(s):  
Konstantinos Zarbalis ◽  
Youngshik Choe ◽  
Julie A Siegenthaler ◽  
Lori A Orosco ◽  
Samuel J Pleasure
Keyword(s):  
Tangential Migration ◽  
Cortical Interneurons

scholarly journals N-Cadherin Sustains Motility and Polarity of Future Cortical Interneurons during Tangential Migration

2013 ◽  
Vol 33 (46) ◽  
pp. 18149-18160 ◽  
Author(s):  
C. Luccardini ◽  
L. Hennekinne ◽  
L. Viou ◽  
M. Yanagida ◽  
F. Murakami ◽  
...  
Keyword(s):  
Tangential Migration ◽  
Cortical Interneurons

scholarly journals BDNF and JNK Signaling Modulate Cortical Interneuron and Perineuronal Net Development: Implications for Schizophrenia-Linked 16p11.2 Duplication Syndrome

2020 ◽  
Author(s):  
Ashleigh Willis ◽  
Judith A Pratt ◽  
Brian J Morris
Keyword(s):  
Cortical Plasticity ◽  
Neurodevelopmental Disorder ◽  
Gabaergic Interneuron ◽  
Perineuronal Net ◽  
Unique Role ◽  
Jnk Signaling ◽  
Developmental Abnormalities ◽  
Cortical Interneuron ◽  
Risk Variants ◽  
Cortical Interneurons

Abstract Schizophrenia (SZ) is a neurodevelopmental disorder caused by the interaction of genetic and environmental risk factors. One of the strongest genetic risk variants is duplication (DUP) of chr.16p11.2. SZ is characterized by cortical gamma-amino-butyric acid (GABA)ergic interneuron dysfunction and disruption to surrounding extracellular matrix structures, perineuronal nets (PNNs). Developmental maturation of GABAergic interneurons, and also the resulting closure of the critical period of cortical plasticity, is regulated by brain-derived neurotrophic factor (BDNF), although the mechanisms involved are unknown. Here, we show that BDNF promotes GABAergic interneuron and PNN maturation through JNK signaling. In mice reproducing the 16p11.2 DUP, where the JNK upstream activator Taok2 is overexpressed, we find that JNK is overactive and there are developmental abnormalities in PNNs, which persist into adulthood. Prefrontal cortex parvalbumin (PVB) expression is reduced, while PNN intensity is increased. Additionally, we report a unique role for TAOK2 signaling in the regulation of PVB interneurons. Our work implicates TAOK2-JNK signaling in cortical interneuron and PNN development, and in the responses to BDNF. It also demonstrates that over-activation of this pathway in conditions associated with SZ risk causes long-lasting disruption in cortical interneurons.

scholarly journals Developmental Characterization of Zswim5 Expression in the Progenitor Domains and Tangential Migration Pathways of Cortical Interneurons in the Mouse Forebrain

2019 ◽  
Author(s):  
Chuan-Chie Chang ◽  
Hsiao-Ying Kuo ◽  
Shih-Yun Chen ◽  
Kuan-Ming Lu ◽  
Weng Lam Fong ◽  
...  
Keyword(s):  
Cell Fate ◽  
Expression Pattern ◽  
Ganglionic Eminence ◽  
Double Labeling ◽  
Tangential Migration ◽  
Cortical Interneurons ◽  
Low Levels ◽  
Migration Pathways

ABSTRACTGABAergic interneurons play an essential role in modulating cortical networks. The progenitor domains of cortical interneurons are localized in developing ventral forebrain, including the medial ganglionic eminence (MGE), caudal ganglionic eminence (CGE), preoptic area (POA) and preoptic hypothalamic border domain (POH). Here, we characterized the expression pattern of Zswim5, an MGE-enriched gene in the mouse forebrain. At E11.5 to E13.5, prominent Zswim5 expression was detected in the subventricular zone (SVZ) of MGE, CGE, POA and POH of ventral telencephalon in which progenitors of cortical interneurons resided. At E15.5 and E17.5, Zswim5 remained detectable in the SVZ of pallidal primordium (MGE). Zswim5 mRNA was markedly decreased after birth and was absent in the adult forebrain. Interestingly, Zswim5 expression pattern resembled the tangential migration pathways of cortical interneurons. Zswim5-positive cells in the MGE appeared to migrate from the MGE through the SVZ of LGE to overlying neocortex. Indeed, Zswim5 was co-localized with Nkx2.1 and Lhx6, markers of progenitos and migratory cortical interneurons. Double labeling showed that Mash1/Ascl1-positive cells did not express Zswim5. Zswim5 expressing cells showed none or at most low levels of Ki67 but co-expressed Tuj1 in the SVZ of MGE. These results suggest that Zswim5 is immediately upregulated as progenitors exiting cell cycle to become postmitotic. Given that recent studies have elucidated that the cell fate of cortical interneurons is determined shortly after postmitotic, the timing of Zswim5 expression in early postmitotic cortical interneurons suggests a potential role of Zswim5 in regulation of neurogenesis and tangential migration of cortical interneurons.

scholarly journals Vascular-derived SPARC and SerpinE1 regulate interneuron tangential migration and maturation

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Matthieu Genestine ◽  
Daisy Ambriz ◽  
Gregg W Crabtree ◽  
Patrick Dummer ◽  
Anna Molotkova ◽  
...  
Keyword(s):  
Critical Role ◽  
Mouse Development ◽  
Paracrine Factors ◽  
Embryonic Mouse ◽  
Tangential Migration ◽  
Mouse Cortex ◽  
Neuropsychiatric Diseases ◽  
Cortical Interneurons ◽  
Progenitor Domain ◽  
Pre Treatment

Cortical interneurons establish inhibitory microcircuits throughout the neocortex and their dysfunction has been implicated in epilepsy and neuropsychiatric diseases. Developmentally, interneurons migrate from a distal progenitor domain in order to populate the neocortex - a process that occurs at a slower rate in humans than in mice. In this study, we sought to identify factors that regulate the rate of interneuron maturation across the two species. Using embryonic mouse development as a model system, we found that the process of initiating interneuron migration is regulated by blood vessels of the medial ganglionic eminence (MGE), an interneuron progenitor domain. We identified two endothelial cell-derived paracrine factors, SPARC and SerpinE1, that enhance interneuron migration in mouse MGE explants and organotypic cultures. Moreover, pre-treatment of human stem cell-derived interneurons (hSC-interneurons) with SPARC and SerpinE1 prior to transplantation into neonatal mouse cortex enhanced their migration and morphological elaboration in the host cortex. Further, SPARC and SerpinE1-treated hSC-interneurons also exhibited more mature electrophysiological characteristics compared to controls. Overall, our studies suggest a critical role for CNS vasculature in regulating interneuron developmental maturation in both mice and humans.

scholarly journals Chondroitin Sulfate Acts in Concert with Semaphorin 3A to Guide Tangential Migration of Cortical Interneurons in the Ventral Telencephalon

2010 ◽  
Vol 20 (10) ◽  
pp. 2411-2422 ◽  
Author(s):  
Geraldine Zimmer ◽  
Sheine M. Schanuel ◽  
Susanne Bürger ◽  
Franco Weth ◽  
André Steinecke ◽  
...  
Keyword(s):  
Chondroitin Sulfate ◽  
Semaphorin 3A ◽  
Ventral Telencephalon ◽  
Tangential Migration ◽  
Cortical Interneurons

scholarly journals Cdk5 Phosphorylation of ErbB4 is Required for Tangential Migration of Cortical Interneurons

2013 ◽  
Vol 25 (4) ◽  
pp. 991-1003 ◽  
Author(s):  
Sonja Rakić ◽  
Shigeaki Kanatani ◽  
David Hunt ◽  
Clare Faux ◽  
Anna Cariboni ◽  
...  
Keyword(s):  
Tangential Migration ◽  
Cortical Interneurons

scholarly journals JNK signaling controls branching, nucleokinesis, and positioning of centrosomes and primary cilia in migrating cortical interneurons

2020 ◽  
Author(s):  
Skye E. Smith ◽  
Nicholas K. Coker ◽  
Eric S. Tucker
Keyword(s):  
Neurological Disorders ◽  
Primary Cilia ◽  
Side Branch ◽  
Intrinsic Activity ◽  
Biological Processes ◽  
Jnk Pathway ◽  
Jnk Signaling ◽  
Cortical Interneurons ◽  
Summary Statement ◽  
Kinetics Of

ABSTRACTAberrant migration of inhibitory interneurons can alter the formation of cortical circuitry and lead to severe neurological disorders including epilepsy, autism, and schizophrenia. However, mechanisms involved in directing the migration of these cells remain incompletely understood. In the current study, we used live-cell confocal microscopy to explore the mechanisms by which the c-Jun NH2-terminal kinase (JNK) pathway coordinates leading process branching and nucleokinesis, two cell biological processes that are essential for the guided migration of cortical interneurons. Pharmacological inhibition of JNK signaling disrupts the kinetics of leading process branching, rate and amplitude of nucleokinesis, and leads to the rearward mislocalization of the centrosome and primary cilium to the trailing process. Genetic loss of Jnk from interneurons corroborates our pharmacological observations and suggests that important mechanics of interneuron migration depend on the intrinsic activity of JNK. These findings suggest that JNK signaling regulates leading process branching, nucleokinesis, and the trafficking of centrosomes and cilia during interneuron migration, and further implicates JNK signaling as an important mediator of cortical development.Summary StatementLoss of JNK signaling reduces growth cone branching frequency, limits interstitial side branch duration, alters rate and amplitude of nucleokinesis, and mislocalizes centrosomes and primary cilia in migrating cortical interneurons.

scholarly journals Developmental characterization of Zswim5 expression in the progenitor domains and tangential migration pathways of cortical interneurons in the mouse forebrain

2020 ◽  
Vol 528 (14) ◽  
pp. 2404-2419
Author(s):  
Chuan‐Chie Chang ◽  
Hsiao‐Ying Kuo ◽  
Shih‐Yun Chen ◽  
Wan‐Ting Lin ◽  
Kuan‐Ming Lu ◽  
...  
Keyword(s):  
Tangential Migration ◽  
Cortical Interneurons ◽  
Migration Pathways
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