What are the molecular and cellular mechanisms by which some babies develop epileptic encephalopathies and autism spectrum disorder? That's what researchers in Canada and France set out to uncover—and they think they've found an answer. It turns out that many of these neurodevelopmental disorders are due to a dysfunction in the development of GABAergic interneurons, cells that are scarce in the brain, but whose inhibitory role is crucial to the proper wiring of the cerebral cortex. In particular, mutations in the TRIO gene disrupt the migration of these interneurons, impairing their ability to integrate properly into circuits and hindering brain development .
That's the finding of a new study by Université de Montréal postdoctoral fellow Lara Eid led by Dr. Elsa Rossignol at the UdeM-affiliated CHU Sainte-Justine, with Dr. Evelyne Bloch-Gallego of Institut Cochin in Paris.
The study appears in Molecular Psychiatry . A unique technique After developing a unique microscopy technique that enables real-time tracking of interneuron movement during the embryonic period, the researchers demonstrated that loss of function of the TRIO gene causes significant difficulties in interneuron migration, a key process in the formation of the cerebral cortex. During normal brain development in an unborn baby, interneurons must leave a deep embryonic structure and travel long distances to reach the developing cortex.
"What we observe in mouse models with interneuron-specific TRIO deletion.
