Reflexes evoked by electrical stimulation of afferent axons in the pudendal nerve under empty and distended bladder conditions in urethane-anesthetized rats

This study examined reflex mechanisms that mediate urinary bladder and external urethral sphincter (EUS) coordination in female Sprague-Dawley urethane-anesthetized rats under empty and distended bladder conditions. The bladder was distended either by a small balloon or a saline filled catheter inserted through the body of the bladder. Stimulation of the entire pudendal nerve elicited short latency (8–12 ms) responses in the EUS and short (3–8 ms) and long latency responses (16–20 ms) in contralateral pudendal nerve. The long latency pudendal–pudendal reflex was reduced by 36.7% in area during bladder distension with the balloon catheter. However, there was no significant change in the area of pudendal–EUS reflex during bladder distension. Peak amplitudes of both reflexes were reduced 32% by bladder distension. The effects of glutamatergic receptor antagonists on the reflexes were also examined. MK801 (0.3–5 mg/kg, i.v.), an N-methyl-d-aspartate glutamatergic receptor antagonist, markedly depressed the pudendal–pudendal reflex, but LY215490 (3 mg/kg, i.v.), an alpha-amino-5-methyl isoxazole-4-propionate antagonist, had a minimal inhibitory effect. Both glutamatergic receptor antagonists significantly suppressed the pudendal–EUS reflex. These results indicate that the EUS is innervated by multiple pathways and that glutamatergic excitatory transmission is important in the neural mechanisms underlying bladder–sphincter coordination in the rat.