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This research investigates the mechanisms by which glutamate influences the migration of GABA interneurons during cortical development.

Glutamate controls vessel-associated migration of GABA interneurons from the pial migratory route via NMDA receptors and endothelial protease activation

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Randomized trial shows glutamate controls GABA interneuron positioning in the cortex, highlighting implications for neonatal treatments.

This research investigates the mechanisms by which glutamate influences the migration of GABA interneurons during cortical development.
Utilized time-lapse recordings to observe GABA interneuron migration along vascular structures.
Performed functional assays and loss-of-function studies in mouse models, including t-PA−/− and Grin1 endothelial invalidation.
Examined the role of NMDA receptors and endothelial proteases MMP-9 and t-PA in the migratory process.
Glutamate enhanced GABA interneuron migration along vessels, mediated by NMDA receptor activation.
In t-PA−/− mice, GABA interneuron positioning was significantly impaired, confirming the enzyme’s role in migration.
Grin1 endothelial invalidation decreased pial migratory route thickness and reduced MMP-9 activity along the route, leading to fewer interneurons in superficial cortical layers.

Léger et al. (2019) studied this question.

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