Voltage-dependent sodium currents (VDNCs) active below or around threshold influence in a critical way the excitable properties of entorhinal cortex (EC) layer II neurons. They include the persistent sodium current (I_NaP) and the resurgent sodium current (I_NaR). Voltage-gated sodium channels of EC layer II cells have previously been reported to show an atypical, "heart-like" pharmacological profile, and such peculiarity has been proposed to reflect specific molecular properties that could influence their ability to generate prominent subthreshold or near-threshold currents. In this study we addressed this point by re-evaluating the pharmacological profile of VDNCs in rat EC layer II neurons. Whole-cell, patch-clamp experiments were carried out both in acutely dissociated neurons and in slices. The transient sodium current (I_NaT) showed a high sensitivity to tetrodotoxin (TTx), with an IC₅₀ of ~7 nM. Instead, zinc ions (Zn²⁺) blocked I_NaT with low potency (IC₅₀ >> 1 mM). Hence, I_NaT showed none of the pharmacological properties typical of cardiac sodium channels. I_NaR was blocked by Zn²⁺ more effectively than I_NaT. Riluzole also differentially affected the various current components: in particular, it reduced maximal I_NaR amplitude to a lesser degree than I_NaT's, and it shifted I_NaR voltage dependence by 5-10 mV in the negative direction. The possible mechanistic bases of the latter phenomena will be discussed in light of the proposed mechanisms of I_NaR generation.