The absence of thyroid hormone-producing follicular cells in the mouse caused by the knockout of both Pax8 allels leads to a complete absence of thyroid hormones T3 (Triiodothyronine) and T4 (Thyroxine) (Mansouri et al., 1998). Here we investigated whether the knockout of the Pax8 transcription factor disturbs the regulation of sodium currents in the Pax8-/- mouse in the same way as induced after blockage of T3 production by Propyl-Thio- Uracil (PTU) (Hoffmann and Dietzel, 2004). Pax8-/- mice showed on the average smaller sizes as their wildtype siblings. Using whole-cell patch-clamp recordings on acutely isolated hippocampal neurons we found smaller sodium current densities in the Pax8-/- mice compared with their heterozygous and wildtype siblings. In contrast the potassium current densities were not significantly affected. Current densities normalized to capacitance of the wildtype mice rose from P1 to P6 from 20pA/pF up to almost 40pA/pF whereas the currents of the knockout animals remained constant at a level of 10pA/pF. In further experiments we plan to investigate which sodium current isoforms are affected and whether the low expression of sodium currents could contribute to the poor survival of the Pax8-/- mice.