Pyramidal neurons in the piriform cortex from olfactory-discrimination trained rats have reduced post- burst after-hyperpolarization (AHP), for three days after learning, and are thus more excitable during this period. Such AHP reduction is due to decreased conductance of one or more of the calcium-dependent potassium currents, the I_AHP and the sI_AHP that mediate the medium and the slow AHP. In the present study we examined which potassium current is reduced by learning, and how the effect of Noradrenalin (NE) on neuronal excitability is modified by such reduction. The small conductance (SK) channels inhibitor, apamin, that selectively blocks the I_AHP, reduced the AHP in neurons from trained, naive and pseudo trained rats to a similar extent, thus maintaining the difference in AHP amplitude between neurons from trained rats and controls. In addition, the protein expression level of the SK1, SK2 and SK3 channels was also similar in all groups. NE, which was shown to enhance the I_AHP while suppressing the SIAHP, reduced the AHP in neurons from controls but enhanced the AHP in neurons from trained. Our data show that learning-induced enhancement of neuronal excitability is not the result of reduction in the I_AHP current. Thus, it is probably mediated by reduction in conductance of the other calcium-dependent potassium current, the sI_AHP. Consequently, the effect of NE on neuronal excitability is reversed. We propose that the change in NE's effect after learning may act to counterbalance learning-induced hyper-excitability and preserve the piriform cortex ability to subserve olfactory-learning.