Stress urinary incontinence (SUI) is a common and bothersome problem among middle-aged women. Various animal models of SUI have been developed to study the pathophysiological process involved in SUI, such as vaginal distention, pudendal nerve injury, or ovariectomy. We have also reported cerebral infarction rats induce not only bladder overactivity, but also SUI. Leak point pressure measurements are the most commonly used methods to evaluate the urethral dysfunction in SUI animal models. Originally, we have developed microtransducer-tipped catheter measurements of urethral activity during sneezing. Extensive our basic research has clarified potential strategies for pharmacotherapy of SUI in the central nervous system. Therapeutic targets include adrenergic and serotonergic (5-HT) receptors in the spinal cord projected from neurons in the locus coeruleus and raphe nucleus, respectively, which stimulate pudendal nerve innervating the external urethral sphincter. Activation of α₁-adrenoceptors, 5-HT_2C, or 5-HT₇ receptors enhances the reflex at the spinal cord level whereas pre- or postsynaptic α₂-adrenoceptors and/or 5-HT_1A receptors inhibit the reflex. In addition, we have reported that stimulation of the spinal μ-opioid receptors may be a new candidate for the treatment of SUI. Thus, we review the recent advances in basic SUI research and potential targets for pharmacotherapy of SUI in the central nervous system.