SPINAL EXPRESSION OF NEUROTROPHIN-3 PREVENTS MUSCULAR CHANGES OF THE URINARY BLADDER AFTER SPINAL CORD CONTUSION IN RATS

after study. Bladder contractions were induced by saline infusion and intravesical pressure (IVP), voided volume and EUS-EMG recorded. Voiding contractions were divided phasic vs nonphasic according to the presence of phasic EUS cycles (one EMG burst followed by a pause = 1 EUS cycle with 1 high frequency IVP oscillation). RESULTS: Intrathecal application of MK-801, a noncompetitive antagonist at the NMDA receptor, was without effect at doses below about 0.1 nmol. At 0.1-3 nmol, MK-801 markedly increased the %age of phasic voiding contractions among all voiding contractions and increase the number of EUS cycles per void four-fold. Characteristics of phasic EUS activity other than EUS cycle number/void did not change (among the durations, root-mean-square amplitudes, and spike frequencies of constituent bursts and pauses). Peak intravesical pressure fell until bladder contractions were completely blocked with intrathecal application of MK-801 at 30-100 nmol. CONCLUSIONS: The increased %age of phasic voiding contractions at moderate doses could represent either conversion of nonphasic to phasic contractions or, if nonphasic and phasic contractions use different neural pathways, a favoring of the phasic pathway. Together with the increase in phasic contractions per void in phasic contractions, a conversion of nonphasic to phasic contractions is supported. That MK-801 blocks both nonphasic and phasic contractions at higher doses indicates that, as in the spinally intact rat, NMDA receptors remain