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Intrinsic excitability (IE) can be defined as an output of action potentials from a given input signal. Changes to the IE of a neuron are an important aspect of the cellular plasticity that underlies learning and memory process. In this study, long-term plastic change in IE of deep dorsal horn neurons (DHNs) was investigated. Associative spike pairing stimulation (PS) induced a long-lasting increase in IE. Buffering intracellular calcium with BAPTA (10 mM) prevented the induction of a long-lasting increase in IE. PS failed to induce a long-lasting increase in IE in the presence of either D-APV (50 μM) or cadmium chloride (100 μM). Apamin (100 nM) partially blocked the induction of a long-lasting increase in IE. This intrinsic plasticity requires a rise in postsynaptic Ca2+ and NMDA receptor activation during the induction period, and this process might be mediated by the down-regulation of small-conductance calcium-dependent potassium (SK) channels. In deep DHNs, PS induced excitatory postsynaptic potential (EPSP)-spike (E-S) potentiation, which increases the firing probability and the number of spikes, by consistent dorsal rootlet stimulation. Under bath application of bicuculline (10 μM) and strychnine (1 μM), PS induced E-S potentiation and long-lasting increases in IE. These results suggest that an increase in IE might underlie E-S potentiation, while a reduction in inhibitory transmission does not contribute to E-S potentiation and long-lasting increases in IE. We conclude that PS enhances the IE of deep DHNs, which may play an important role in spinal processing of nociceptive information.