Journal of Physiology 534, 763-776 (2001) At a number of places β should have appeared asα: On page 763, 2nd paragraph, 3rd line, β subunit should have appeared asα subunit. 5th line, 1β:1Naβ1.1:1Naβ2.1 should have appeared as 1α:1Naβ1.1:1Naβ2.1 7th line,β subunit should have appeared asα subunit. 10th line,β subunits should have appeared asα subunits. 16th line,β subunits should have appeared asα subunits. 4th paragraph, 2nd line,β subunits should have appeared asα subunits. On page 764, 1st paragraph, 9th line,β subunits should have appeared asα subunits. 2nd paragraph last lineβ subunits should have appeared asα subunits. Thus the Introduction should have appeared as follows: Voltage-gated sodium channels play an important role in excitable cells. They mediate an increase in Na+ ion permeability thereby transmitting depolarising impulses rapidly throughout cells and cell networks (Catterall, 1984). These molecules are also thought to perform a pivotal role during CNS development since action potential propagation and excitatory transmission are vital in the maturation of neuronal morphological, electrophysiological and molecular properties (Shatz, 1990; Fields & Nelson, 1992; Goodman & Shatz, 1993). Although current evidence strongly supports the functional importance of sodium channels during development, little information presently exists concerning their molecular properties. Within the mature CNS, voltage-gated Na+ channels have been shown to be composed of three glycoprotein subunits, a pore-forming α subunit and two auxiliary subunits Naβ1.1 and Naβ2.1, which assemble with a subunit stoichiometry of 1α:1Naβ1.1:1Naβ2.1 (Messner & Catterall, 1985). Although ion permeability and voltage sensing is primarily determined by the α subunit, β subunits are important modulators of Na+ channel function. For example, co-expression studies of Naβ1.1 with either neuronal or skeletal muscle α subunits show that this auxiliary subunit increases current density, accelerates gating kinetics and shifts the steady-state inactivation curve in the hyperpolarizing direction (Isom et al. 1992; Bennett et al. 1993; Cannon et al. 1993; Patton et al. 1994). Similarly, expression of Naβ2.1 with neuronal α subunits in oocytes increases current amplitude, modulates gating and increases membrane capacitance (Isom et al. 1995). In previous studies the expression of Naβ1.1 mRNA in the rat brain has been shown to be a postnatal phenomena. No expression of Naβ1.1 mRNA has been observed in the rat embryo (Patton et al. 1994) and expression has been shown to steadily increase after day 1 (P1), reaching a plateau 2-3 weeks after birth and persisting into adulthood (Sashihara et al. 1995). Northern blot studies have shown that Naβ2.1 mRNA can be detected from embryonic day 20 (E 20) onwards (Isom et al. 1995), whilst specific antibodies recognise Naβ2.1 from P7 onwards (Wood et al. 1995). Despite this apparent lack of β subunit expression during embryonic development, sodium channel α subunits are expressed and functional Na+ currents can be detected (Mandler et al. 1990). For example, the Nav1.3 subunit has been shown to be a major embryonic voltage-gated sodium channel, expressed extensively during prenatal development. Similarly Nav1.6 mRNA is detectable throughout both development and adulthood (Beckh et al. 1989; Brysch et al. 1991; Felts et al. 1997). On the basis of these findings, therefore, it would appear that other embryonic β subunits may exist, or alternatively, these embryonic α subunits function in the CNS independently of associated β subunits. With regard to this former suggestion, although Naβ1.1-specific antibodies have been unable to detect specific immunoreactivity in the rat embryo, these antibodies were cross-reactive with a species of approximately 42 kDa suggesting that alternative Naβ1.1-like subunits may be present (Sutkowski & Catterall, 1990). Indeed, Kazen-Gillespie et al. (2000) have recently cloned a Naβ1.1 splice variant, Naβ1.1A, which is expressed in rat embryo, but whose expression falls following birth. Furthermore, we have recently identified a novel β subunit, β3, related to Naβ1.1 exhibiting 50 % homology (Morgan et al. 2000). Since Naβ1.1 and β3 show a complimentary pattern of distribution in the adult rat, in the present study we have compared the ontogeny of β3 with other β subunits and embryonic α subunits. On page 773, Figure 10 legend, 7th line, Nav1.3, •; Nav1.3 +β3, ○ should have appeared as Nav1.3, ○; Nav1.3 +β3, •. On page 774, 3rd paragraph, 2nd line, above β subunits should have appeared as above α subunits 6th paragraph, 4th line, embryonic β subunits should have appeared as embryonic α subunits. On page 775, 1st paragraph, 13th line, couple to β subunits should have appeared as couple to α subunits.