Lack of thyroid hormone (TH) in the critical developmental period of the inner ear between E17 and P12 leads to morphological and functional deficits in the organ of Corti and the auditory pathway. To investigate the effects of TH on inner hair cells (IHC) we used hypothyroid rats treated with the thyreostatic drug methimazol during pre- and postnatal life. Whole-cell Ca2+ and K+ currents and Ca2+ action potentials were measured in hypothyroid animals and controls. Ca2+ channel currents (10 mM Ba2+ as charge carrier; IBa) showed a developmental peak of 420 pA between P9-P11 and declined to mature values of 180 pA by P19. IBa of hypothyroid IHCs showed an increased peak of 825 pA at P19 and a delayed decline to reduced mature values of 144 pA at P32. IHCs of hypothyroid rats did not express the BK current, which is up-regulated in control IHCs at P12, before P28. After that, some hypothyroid IHCs showed a BK-like current with reduced amplitude. Delayed-rectifier K+ currents were unaffected by lack of TH. In conclusion, the expression levels of both the Cav1.3 and the BK channel are regulated by TH. Hypothyroid IHCs persisted generating Ca2+ action potentials until P19 most likely due to lack of BK that normally shunts spiking activity. Supported by DFG En294/2-4, Kni316/4-1, Fortuene 1446-0-0