Mutations in FGF14, which encodes intracellular fibroblast growth factor 14 (iFGF14), have been linked to spinocerebellar ataxia type 27 (SCA27), a multisystem disorder associated with deficits in motor coordination and cognitive function. Mice lacking iFGF14 (Fgf14-/-) display similar phenotypes, and we have previously shown that the deficits in motor coordination reflect reduced excitability of cerebellar Purkinje neurons, owing to a hyperpolarizing shift in the voltage-dependence of voltage-gated Na+ (Nav) current steady-state inactivation. Here, we present the results of experiments designed to test the hypothesis that loss of iFGF14 also attenuates the intrinsic excitability of mature hippocampal pyramidal neurons. Current-clamp recordings from CA1 pyramidal neurons in acute in vitro slices, however, revealed that evoked repetitive firing rates were higher in Fgf14-/- than in wild type (WT) cells. Also, in contrast with Purkinje neurons, voltage-clamp recordings demonstrated that the loss of iFGF14 did not affect the voltage dependence of steady-state inactivation of the Nav currents in CA1 pyramidal neurons. In addition, in contrast with results reported for neonatal (rat) hippocampal pyramidal neurons in dissociated cell culture, immunohistochemical experiments revealed that loss of iFGF14 does not disrupt the localization or alter the normalized distribution of α-Nav1.6 or α-ankyrin G labeling along the axon initial segments (AIS) of mature hippocampal CA1 neurons in situ. However, the integrated intensities of α-Nav1.6 labeling were significantly higher along the AIS of Fgf14-/-, compared with WT, adult hippocampal CA1 pyramidal neurons, consistent with the marked increase in the excitability of CA1 neurons with the loss of iFGF14.