The multiplex role of cadherin-based adhesion complexes during development of pallial
excitatory neurons has been thoroughly characterized. In contrast, much less is known
about their function during interneuron development. Here, we report that conditional
removal of N-cadherin (Cdh2) from postmitotic neuroblasts of the subpallium results
in a decreased number of Gad65-GFP-positive interneurons in the adult cortex. We also
found that interneuron precursor migration into the pallium was already delayed at
E14. Using immunohistochemistry and TUNEL assay in the embryonic subpallium, we excluded
decreased mitosis and elevated cell death as possible sources of this defect. Moreover,
by analyzing the interneuron composition of the adult somatosensory cortex, we uncovered
an unexpected interneuron-type-specific defect caused by Cdh2-loss. This was not due
to a fate-switch between interneuron populations or altered target selection during
migration. Instead, potentially due to the migration delay, part of the precursors
failed to enter the cortical plate and consequently got eliminated at early postnatal
stages. In summary, our results indicate that Cdh2-mediated interactions are necessary
for migration and survival during the postmitotic phase of interneuron development.
Furthermore, we also propose that unlike in pallial glutamatergic cells, Cdh2 is not
universal, rather a cell type-specific factor during this process.
