Heterozygous loss-of-function SCN1A mutations cause Dravet syndrome, an epileptic encephalopathy of infancy that exhibits variable clinical severity. We utilized a heterozygous Scn1a knockout (Scn1a^+/−) mouse model of Dravet syndrome to investigate the basis for phenotype variability. These animals exhibit strain-dependent seizure severity and survival. Scn1a^+/− mice on strain 129S6/SvEvTac (129.Scn1a^+/−) have no overt phenotype and normal survival compared with Scn1a^+/− mice bred to C57BL/6J (F1.Scn1a^+/−) that have severe epilepsy and premature lethality. We tested the hypothesis that strain differences in sodium current (I_Na) density in hippocampal neurons contribute to these divergent phenotypes. Whole-cell voltage-clamp recording was performed on acutely-dissociated hippocampal neurons from postnatal days 21–24 (P21–24) 129.Scn1a^+/− or F1.Scn1a^+/− mice and wild-type littermates. I_Na density was lower in GABAergic interneurons from F1.Scn1a^+/− mice compared to wild-type littermates, while on the 129 strain there was no difference in GABAergic interneuron I_Na density between 129.Scn1a^+/− mice and wild-type littermate controls. By contrast, I_Na density was elevated in pyramidal neurons from both 129.Scn1a^+/− and F1.Scn1a^+/− mice, and was correlated with more frequent spontaneous action potential firing in these neurons, as well as more sustained firing in F1.Scn1a^+/− neurons. We also observed age-dependent differences in pyramidal neuron I_Na density between wild-type and Scn1a^+/− animals. We conclude that preserved I_Na density in GABAergic interneurons contributes to the milder phenotype of 129.Scn1a^+/− mice. Furthermore, elevated I_Na density in excitatory pyramidal neurons at P21–24 correlates with age-dependent onset of lethality in F1.Scn1a^+/− mice. Our findings illustrate differences in hippocampal neurons that may underlie strain- and age-dependent phenotype severity in a Dravet syndrome mouse model, and emphasize a contribution of pyramidal neuron excitability.