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[Display omitted] • Moxibustion prevented the development of detrusor overactivity in SCI rats. • Moxibustion attenuated the expression of M2 muscarinic receptor subtype in the bladder of SCI rats. • The M2 receptor antagonist methoctramine hemihydrate mimics moxibustion-induced improvement of urodynamic parameters and afferent nerve activity, and the muscarinic receptor agonist oxotremorine methiodide reverses the beneficial effect of moxibustion. • Moxibustion reduced the release of ATP and the expression of P2X3 in the M2 receptor-mediated micturition reflex pathway. Activation of muscarinic receptors located in bladder sensory pathways is generally considered to be the primary contributor for driving the pathogenesis of neurogenic detrusor overactivity following spinal cord injury. The present study is undertaken to examine whether moxibustion improves neurogenic detrusor overactivity via modulating the abnormal muscarinic receptor pathway. Female Sprague-Dawley rats were subjected to spinal cord injury with T9-10 spinal cord transection. Fourteen days later, animals were received moxibustion treatment for one week. Urodynamic parameters and pelvic afferents discharge were measured. Adenosine triphosphate (ATP) content in the voided cystometry fluid was determined. Expressions of M2, M3, and P2X3 receptors in the bladder mucosa were evaluated. Moxibustion treatment prevented the development of detrusor overactivity in spinal cord injury rats, with an increase in the intercontraction interval and micturition pressure threshold and a decrease in afferent activity during filling. The expression of M2 was markedly suppressed by moxibustion, accompanied by a reduction in the levels of ATP and P2X3. M2 receptor antagonist methoctramine hemihydrate had similar effects to moxibustion on bladder function and afferent activity, while the M2-preferential agonist oxotremorine methiodide abolished the beneficial effects of moxibustion. Moxibustion is a potential candidate for treating neurogenic bladder overactivity in a rat model of spinal cord injury, possibly through inhibiting the M2/ATP/P2X3 pathway. [ABSTRACT FROM AUTHOR]