Deletion of Alg13 disrupts postnatal development and migration of GABAergic cortical interneurons

Abnormal cortical neuron development is closely associated with various neurological disorders. Deletion of the Alg13 gene has been identified as strongly associated with epilepsy susceptibility and seizure severity in mice. Similar deletions have also been observed in patients with epilepsy, indicating that Alg13 may play a critical role in cortical interneuron development.

Immunofluorescence analysis was used to assess the effects of Alg13 deletion on the distribution and migration of interneurons in the cerebral cortex of postnatal mice. Transcriptome sequencing was performed to identify genes involved in neuronal development, and the findings were validated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR).

Deletion of Alg13 significantly influenced the spatiotemporal distribution of cortical interneurons in postnatal mouse brains. The migratory capacity of interneuron subtypes was markedly reduced in Alg13-deficient mice, indicating a potential increase in epilepsy susceptibility and seizure severity. Transcriptome sequencing and RT-qPCR validation identified three genes, Ndn, Dynlt1b, and C3, that were associated with the development of inhibitory interneurons.

Alg13 regulates postnatal interneuron development, and its deletion may contribute to epilepsy-related pathophysiology. These results enhance understanding of the molecular mechanisms underlying epilepsy and provide a potential experimental foundation and novel therapeutic targets for the management of Alg13-associated refractory seizures, thereby advancing knowledge of interneuron developmental regulation.