Recently, FDA has approved the sacral nerve stimulation technology for three types of indications: persistent urge incontinence, intractable urgency and urinary frequency syndrome and non-obstructive chronic urinary retention. With continuous technical advancement, electrical stimulation is becoming an important clinical treatment for patients with bladder and urethra dysfunction. However, the traumatic aspect and tolerance of such treatment limited its clinical applications. By far, few studies on the electric nerve stimulation treatment of DCP have been reported. The urodynamics and exact mechanisms of electrical stimulation have not been studied. In 1980, supra-pubic surface electrical stimulation was firstly applied on interstitial cystitis to decrease the pain and increase the bladder capacity. In 2004, Yokozuka placed electrical stimulation electrodes on the dorsal S2, S4 sacral foramina surface to treat 18 patients with refractory urinary incontinence, and achieved desired results. However, application of this technology on DCP has been rarely reported and the underlying mechanism is still unknown. In this study, we first developed a rat model of DCP and investigated the effects of in vivo electrical stimulation on the function of detrusor and the possible mechanisms. The results obtained in this study could provide scientific foundations for electrical stimulation treatment of DCP. Clinical and experimental studies on the treatment of DCP have been mainly focusing on the acceleration of nerve regeneration and delay of the detrusor atrophy. The main treatment for DCP is pharmacotherapy including blood glucose control, nerve nourishment, promotion of bladder contraction and circulation and application of antibiotics. Although the treatment of diabetic neurogenic dysfunctions of micturition can protect upper urinary tract function, the DCP could be recurrent. During the past decades, a number of studies have investigated the therapeutic efficacy of neuromodulation of the bladder and established an artificial somatic-visceral reflex pathway as a relatively effective means for neurogenic bladder. It appears that modulation of spinal cord reexes and brain networks is involved in the neuromodulation, but the exact mechanism AbMole Isovitexin remains to be elucidated Neuromodulation predominantly involves the areas associated with sensorimotor learning, which might become progressively less active during the course of chronic neuromodulation. Moreover, the sympathetic nervous system might play a role as low-frequency pudendal nerve stimulation occurs in cats with chronic spinal cord injury. It has been well demonstrated that sensory stimulation of the abdominal skin by pinching inhibits gastric motility via increasing sympathetic efferent activity in rats. Some studies also reported that intravesical electrical stimulation can ameliorate children��s bladder contractile function, and one previous study showed that electrical stimulation of the stomach could contribute to improving the gastroparesis in patients with diabetes. However, non-invasive electrical stimulation has not been applied to improve the voiding dysfunction in rats with DCP. Therefore, in this study, we applied non-invasive electrical stimulation in the surface to improve the voiding dysfunction in rats with DCP, and explored the underlying mechanisms. cAMP is an important intracellular second messenger of badrenergic nerve and several NANC nerve pathways.