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Autonomous and non-autonomous roles for ephrin-B in interneuron migration.
Asghar Talebian1, Rachel Britton1, Simon Ammanuel2
1Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Developmental Biology
|September 27, 2017
Summary
Ephrin-B reverse signaling is crucial for interneuron migration into the neocortex, impacting cortical excitability and leading to seizures. Ephrin-B also acts as a ligand, guiding interneuron migration for brain homeostasis.
Area of Science:
- Neuroscience
- Developmental Biology
- Molecular Biology
Background:
- Ephrin-B/EphB signaling is vital in excitatory neurons.
- Its role in inhibitory neurons remains largely unexplored.
Purpose of the Study:
- Investigate the function of ephrin-B reverse signaling in interneuron migration.
- Determine the roles of ephrin-B in cortical development and function.
Main Methods:
- Utilized ephrin-B conditional triple mutant (EfnB1/B2/B3 TMlz) mice.
- Employed a forebrain inhibitory neuron-specific Cre driver.
- Analyzed interneuron migration, cortical excitability, and seizure phenotypes.
Main Results:
- Inhibitory neuron deletion of EfnB genes reduced interneuron migration and caused abnormal cortical excitability and seizures.
- Mutations confirmed the importance of ephrin-B reverse signaling in migration and excitability.
- Ephrin-B2 in radial glial cells acts as a ligand, essential for GAD65-positive interneuron migration.
Conclusions:
- Ephrin-B molecules play dual receptor-like and ligand-like roles in interneuron migration.
- These functions are critical for neocortical interneuron population and excitatory/inhibitory (E/I) homeostasis.
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