In the protochordate Halocynthia roretzi, voltage-activated sodium current undergoes a change in kinetics within 48 hr of fertilization. Molecular cloning and microinjection of antisense DNA into single cells suggest that the kinetic changes are due to the increased expression of a putative neural-specific sodium channel gene, TuNa I. TuNa I gene transcription is first induced in late stage gastrulae, preceding the appearance of the rapidly inactivating sodium current unique to neural cells. In cleavage-arrested and intact embryos, cell interactions between specific animal and vegetal blastomeres are required for induction of TuNa I gene expression. Our results implicate cell contact, prior to neurulation, as a mechanism for selectively activating the TuNa I gene expressed in cells of the neural lineage.