Acute unilateral ureteral distension inhibits glutamate-dependent spinal pelvic-urethra reflex potentiation via GABAergic neurotransmission in anesthetized rats

The effects of an acute increase in intraureteral pressure ( IUP) on pelvic- urethra reflex potentiation were examined in urethane- anesthetized rats by recording the external urethral sphincter electromyogram activities evoked by the pelvic afferent stimulation. Compared with a single action potential elicited by the test stimulation ( TS; characterized by an intensity that evoked a constant reflex response without facilitation, 1/ 30 Hz, 1.03 +/- 0.12 spikes/ stimulation, n = 7), the repetitive stimulation [ RS; identical stimulation intensity as the TS ( 1 Hz)] significantly induced spinal reflex potentiation ( SRP; 16.90 +/- 2.00 spikes/ stimulation, P < 0.01, n = 7). Such SRP was significantly attenuated by intrathecal 2,3- dihydroxy- 6- nitro- 7- sulfamoyl- benzo ( F) quinoxaline [ NBQX; a glutamatergic alpha- amino- 3- hydroxy- 5- methyl4- isoxazoleproprionat ( AMPA) receptor antagonist] and D- 2- amino5- phosphonovalerate [ APV; a glutamatergic N- methyl- D- aspartate ( NMDA) antagonist; the spike number per stimulation: 11.0 +/- 0.70 for NBQX, 1.01 +/- 0.30 for APV, and 16.90 +/- 2.0 for RS, respectively, n = 7, P < 0.01]. Acute stepwise elevations of IUP gradually attenuated and eventually abolished the RS- induced SRP ( 16.80 +/- 1.30, 17.00 +/- 1.30, 16.30 +/- 1.30, 10.50 +/- 1.80, 8.80 +/- 1.90, 3.50 +/- 1.60, 0.80 +/- 0.20, 0.70 +/- 0.20, and 0.20 +/- 0.10 spikes/ stimulation at intraureteral pressure of 0, 2.5, 5, 7.5, 10, 12.5, 15, 17.5, and 20 cmH2O, respectively, n = 7). Intrathecal NMDA ( a glutamatergic NMDA receptor agonist) and bicuculline ( a GABA receptor antagonist) both reversed the abolition of RS- induced SRP caused by unilateral ureteral distension ( 14.0 +/- 4.04 and 8.00 +/- 1.53 spikes/ stimulation, respectively, n = 7, P < 0.01). All the results suggested unilateral ureteral distension might compensatorily relax the urethra via GABAergic inhibition of NMDA- dependent SRP.