ArticleFrontiers in neuroscience2022
Modifying PCDH19 levels affects cortical interneuron migration.
Article in Frontiers in neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 17 citations in OpenAlex.
- A data-driven framework linking the connectome to spatial gene expression gradients inspired by chemoaffinity theory.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Neurotrophin-3 produced by motor neurons non-cell autonomously regulate the development of pre-motor interneurons in the developing spinal cord.bioRxiv : the preprint server for biology · 2026Article
- Shared Disease Mechanisms in Neurodevelopmental Disorders: A Cellular and Molecular Biology Perspective.Brain sciences · 2025Review
- Triplication of theGenes · 2024Article
- Altered socio-affective communication and amygdala development in mice with protocadherin10-deficient interneurons.Open biology · 2024Article
- The Interplay of Sports and Nutrition in Neurological Health and Recovery.Journal of clinical medicine · 2024Review
- Host brain environmental influences on transplanted medial ganglionic eminence progenitors.Scientific reports · 2024Article
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- Influence ofFrontiers in genetics · 2023Article
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PCDH19 is a transmembrane protein and member of the protocadherin family. It is encoded by the X-chromosome and more than 200 mutations have been linked to the neurodevelopmental PCDH-clustering epilepsy (PCDH19-CE) syndrome. A disturbed cell-cell contact that arises when random X-inactivation creates mosaic absence of PCDH19 has been proposed to cause the syndrome. Several studies have shown roles for PCDH19 in neuronal proliferation, migration, and synapse function, yet most of them have focused on cortical and hippocampal neurons. As epilepsy can also be caused by impaired interneuron migration, we studied the role of PCDH19 in cortical interneurons during embryogenesis. We show that cortical interneuron migration is affected by altering PCDH19 dosage by means of overexpression in brain slices and medial ganglionic eminence (MGE) explants. We also detect subtle defects when PCDH19 expression was reduced in MGE explants, suggesting that the dosage of PCDH19 is important for proper interneuron migration. We confirm this finding
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