This study examined the role of the brain stem in inhibition of bladder reflexes induced by tibial nerve stimulation (
TNS) in α-
chloralose-anesthetized decerebrate cats. Repeated cystometrograms (CMGs) were performed by infusing saline or 0.25%
acetic acid (AA) to elicit normal or
overactive bladder reflexes, respectively.
TNS (5 or 30 Hz) at three times the threshold (3T) intensity for inducing toe movement was applied for 30 min between CMGs to induce post-
TNS inhibition or applied during the CMGs to induce acute
TNS inhibition. Inhibition was evident as an increase in bladder capacity without a change in amplitude of bladder contractions.
TNS applied for 30 min between saline CMGs elicited prolonged (>2 h) poststimulation inhibition that significantly (P < 0.05) increased bladder capacity to 30-60% above control; however,
TNS did not produce this effect during AA irritation.
TNS applied during CMGs at 5 Hz but not 30 Hz significantly (P < 0.01) increased bladder capacity to 127.3 ± 6.1% of saline control or 187.6 ± 5.0% of AA control. During AA irritation,
naloxone (an
opioid receptor antagonist) administered intravenously (1 mg/kg) or directly to the surface of the rostral brain stem (300-900 μg) eliminated acute
TNS inhibition and significantly (P < 0.05) reduced bladder capacity to 62.8 ± 22.6% (intravenously) or 47.6 ± 25.5% (brain stem application). Results of this and previous studies indicate 1) forebrain circuitry rostral to the pons is not essential for
TNS inhibition; and 2)
opioid receptors in the brain stem have a critical role in
TNS inhibition of
overactive bladder reflexes but are not involved in inhibition of normal bladder reflexes.