Endothelial cell-derived GABA signaling modulates neuronal migration and postnatal behavior View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-02

AUTHORS

Suyan Li, Peeyush Kumar T, Sampada Joshee, Timo Kirschstein, Sivan Subburaju, Jahan S Khalili, Jonas Kloepper, Chuang Du, Abdallah Elkhal, Gábor Szabó, Rakesh K Jain, Rüdiger Köhling, Anju Vasudevan

ABSTRACT

The cerebral cortex is essential for integration and processing of information that is required for most behaviors. The exquisitely precise laminar organization of the cerebral cortex arises during embryonic development when neurons migrate successively from ventricular zones to coalesce into specific cortical layers. While radial glia act as guide rails for projection neuron migration, pre-formed vascular networks provide support and guidance cues for GABAergic interneuron migration. This study provides novel conceptual and mechanistic insights into this paradigm of vascular-neuronal interactions, revealing new mechanisms of GABA and its receptor-mediated signaling via embryonic forebrain endothelial cells. With the use of two new endothelial cell specific conditional mouse models of the GABA pathway (Gabrb3ΔTie2-Cre and VgatΔTie2-Cre), we show that partial or complete loss of GABA release from endothelial cells during embryogenesis results in vascular defects and impairs long-distance migration and positioning of cortical interneurons. The downstream effects of perturbed endothelial cell-derived GABA signaling are critical, leading to lasting changes to cortical circuits and persistent behavioral deficits. Furthermore, we illustrate new mechanisms of activation of GABA signaling in forebrain endothelial cells that promotes their migration, angiogenesis and acquisition of blood-brain barrier properties. Our findings uncover and elucidate a novel endothelial GABA signaling pathway in the CNS that is distinct from the classical neuronal GABA signaling pathway and shed new light on the etiology and pathophysiology of neuropsychiatric diseases, such as autism spectrum disorders, epilepsy, anxiety, depression and schizophrenia. More... »

PAGES

221

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/cr.2017.135

DOI

http://dx.doi.org/10.1038/cr.2017.135

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1092457631

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29086765


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423 schema:name Laboratory of Molecular Biology and Genetics, Department of Gene Technology and Developmental Neurobiology, Institute of Experimental Medicine, 1083 Budapest, Hungary
424 rdf:type schema:Organization
425 https://www.grid.ac/institutes/grid.429997.8 schema:alternateName Tufts University
426 schema:name Department of Neuroscience, Tufts University School of Medicine, Boston, MA 02148, USA;
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428 https://www.grid.ac/institutes/grid.62560.37 schema:alternateName Brigham and Women's Hospital
429 schema:name Department of Surgery, Harvard Medical School, Boston, MA 02115, USA;
430 Division of Transplantation, Brigham and Women's Hospital, 221 Longwood Avenue, EBRC 309, Boston, MA 02115, USA;
431 rdf:type schema:Organization
 




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