Voltage-gated sodium channels (VGSC) play an important role in the initiation and propagation of action potentials in vertebrate cranial nerves. To investigate the role of zebrafish voltage-gated sodium channel member scn1Laa in cranial nerves, the CRISPR/Cas9 approach was used to establish a stable hereditary scn1Laa-deficient (scn1Laa^-/-) zebrafish without significant effect on growth. Compared with wild-type siblings, there were more GABAergic neurons (inhibitory neurons) in scn1Laa-deficient larvae at 5 dpf (5 days post-fertilization), while glutamatergic (excitatory neurons) and mature neurons were significantly reduced. Besides, cell proliferation in the brain was also reduced at 5 dpf. The movement of scn1Laa-deficient zebrafish at 5 or 90 dpf was more active than that of wild-type siblings at the same time, and the burst movement of scn1Laa-deficient zebrafish was observed at 90 dpf. These results showed that loss of scn1laa made excitatory neurons (glutamatergic neurons) decrease and reduced cell proliferation of cranial nerve, which affected the discharge of peripheral nerve, causing motor nerve dysfunction and abnormal motor behavior. Above all, the voltage-gated sodium channel scn1Laa participates in the development and functional maintenance of the zebrafish cranial nerve and indirectly participates in the regulating behavior with limited influence on body growth. At the same time, this research also lays the foundation for further exploration of voltage-gated sodium channels in the cranial nerves.