Autonomous and non-autonomous roles for ephrin-B in interneuron migration
Autor: | Shari G. Birnbaum, Francis Sprouse, Jay R. Gibson, Mark Henkemeyer, Gábor Szabó, Asim Kumar Bepari, Rachel Britton, Asghar Talebian, Simon Ammanuel, Nobuaki Tamamaki |
---|---|
Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Neocortex Biology Inhibitory postsynaptic potential Ligands Models Biological Article Interneuron migration 03 medical and health sciences Mice Prosencephalon Cell Movement Interneurons medicine Ephrin Animals Pseudopodia Molecular Biology Point mutation Neural Inhibition Cell Biology Anatomy 030104 developmental biology medicine.anatomical_structure nervous system Forebrain Mutation Excitatory postsynaptic potential Female Neuroscience Ephrins Intracellular Gene Deletion Developmental Biology |
Zdroj: | Developmental biology. 431(2) |
ISSN: | 1095-564X |
Popis: | While several studies indicate the importance of ephrin-B/EphB bidirectional signaling in excitatory neurons, potential roles for these molecules in inhibitory neurons are largely unknown. We identify here an autonomous receptor-like role for ephrin-B reverse signaling in the tangential migration of interneurons into the neocortex using ephrin-B (EfnB1/B2/B3) conditional triple mutant (TMlz) mice and a forebrain inhibitory neuron specific Cre driver. Inhibitory neuron deletion of the three EfnB genes leads to reduced interneuron migration, abnormal cortical excitability, and lethal audiogenic seizures. Truncated and intracellular point mutations confirm the importance of ephrin-B reverse signaling in interneuron migration and cortical excitability. A non-autonomous ligand-like role was also identified for ephrin-B2 that is expressed in neocortical radial glial cells and required for proper tangential migration of GAD65-positive interneurons. Our studies thus define both receptor-like and ligand-like roles for the ephrin-B molecules in controlling the migration of interneurons as they populate the neocortex and help establish excitatory/inhibitory (E/I) homeostasis. |
Databáze: | OpenAIRE |
Externí odkaz: |