Loss of Alg13 Impairs Postnatal GABAergic Cortical Interneuron Development

Abnormal development of cortical neurons may be closely associated with the presence of neurological disorders, and deletion of the Alg13 gene was strongly associated with epilepsy susceptibility and seizure severity in mice. And the deletion of Alg13 gene is also found in some epileptic patients, which may prove that Alg13 gene plays a role in the development of cortical interneurons. Methods We used immunofluorescence to observe the effects of Alg13 deletion on the distribution and migration of interneurons in the cerebral cortex of postnatal mice, and applied transcriptome sequencing to identify neuronal developmental genes and verified the results using RT-qPCR. Results Alg13 deletion plays a key role in the spatiotemporal distribution of cortical interneurons in the mouse cerebral cortex by establishing an Alg13-deficient mouse model by immunofluorescence, and that the migratory ability of interneuron subtypes in mice was also significantly inhibited by Alg13 deletion, which may increase the susceptibility to epilepsy and the severity of seizures. By transcriptome sequencing as well as RT-qPCR we verified three genes associated with inhibitory interneuron development, Ndn, Dynlt1b, and C3. Conclusions Abnormal development of interneurons may be regulated by Alg13, thus causing epilepsy-related disorders, which will help to further understand the pathogenesis and mechanisms of epilepsy, with a view to providing experimental basis and new therapeutic targets for the clinical application of controlling Alg13-associated refractory seizures, and enriching the understanding of the regulatory mechanisms of interneuron development.