Bladder small DRG neurons, which are putative nociceptors pivotal to urinary bladder function, express more than a dozen different ionic membrane mechanisms: ion channels, pumps and exchangers. Small-conductance Ca²⁺-activated K⁺ (SKCa) channels which were earlier thought to be gated solely by intracellular Ca²⁺ concentration ([Ca\]_i ) have recently been shown to exhibit inward rectification with respect to membrane potential. The effect of SK_Ca inward rectification on the excitability of these neurons is unknown. Furthermore, studies on the role of K_Ca channels in repetitive firing and their contributions to different types of afterhyperpolarization (AHP) in these neurons are lacking. In order to study these phenomena, we first constructed and validated a biophysically detailed single compartment model of bladder small DRG soma constrained by physiological data. The model includes twenty-two major known membrane mechanisms along with intracellular Ca²⁺ dynamics comprising Ca²⁺ diffusion, cytoplasmic buffering, and endoplasmic reticulum (ER) and mitochondrial mechanisms. Using modelling studies, we show that inward rectification of SK_Ca is an important parameter regulating neuronal repetitive firing and that its absence reduces action potential (AP) firing frequency. We also show that SK_Ca is more potent in reducing AP spiking than the large-conductance K_Ca channel (BK_Ca) in these neurons. Moreover, BK_Ca was found to contribute to the fast AHP (fAHP) and SK_Ca to the medium-duration (mAHP) and slow AHP (sAHP). We also report that the slow inactivating A-type K⁺ channel (slow KA) current in these neurons is composed of 2 components: an initial fast inactivating (time constant ~ 25-100 ms) and a slow inactivating (time constant ~ 200-800 ms) current. We discuss the implications of our findings, and how our detailed model can help further our understanding of the role of C-fibre afferents in the physiology of urinary bladder as well as in certain disorders.