Expression of the newly identified beta3 subunit of the voltage-sensitive sodium channel in Xenopus oocytes inactivates channel opening more slowly than the beta1 subunit.
The voltage-sensitive sodium channel confers electrical excitability on neurons, a fundamental property required for higher processes including cognition. The ion-conducting alpha-subunit of the channel is regulated by two known auxiliary subunits, beta1 and beta2. We have identified rat and human forms of an additional subunit, beta3. It is most closely related to beta1 and is the product of a separate gene localized to human chromosome 11q23.3. When expressed in Xenopus oocytes, beta3 inactivates sodium channel opening more slowly than beta1 does. Structural modeling has identified an amino acid residue in the putative alpha-subunit binding site of beta3 that may play a role in this difference. The expression of beta3 within the central nervous system differs significantly from beta1. Our results strongly suggest that beta3 performs a distinct neurophysiological function.
Morgan et al. (Fri,) reported a other. beta3 subunit expression vs. beta1 subunit was evaluated on sodium channel opening inactivation kinetics. Expression of the newly identified beta3 subunit of the voltage-sensitive sodium channel in Xenopus oocytes inactivates channel opening more slowly than the beta1 subunit.