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Electrical stimulation of the urethral sensory pudendal nerve in decerebrate or acute spinal cats was used to evoke micturition reflexes in animals that failed to respond to bladder distension. In the decerebrate animals, stimulation of urethral afferents evoked voiding characterized by a large bladder pressure increase coordinated with a simultaneous decrease in external urethral sphincter activity. In animals in which the spinal cord was transected between T10 and L6, electrical stimulation of the urethral afferents evoked small increases in bladder pressure that were insufficient to expel fluid but the contractions were coordinated with a decrease in external urethral sphincter activity. It was concluded that in addition to interacting with spinobulbospinal micturition pathways, urethral pudendal afferents may have direct access to a spinal circuitry that can coordinate bladder and sphincter activity.

Membrane electrical properties of motoneurons innervating the striated muscle of the external urethral and anal sphincters were examined in the decerebrate cat. Both populations of motoneurons had similar electrical properties (mean pooled values; conduction velocity 48 m/s, membrane time constant 3.3 ms, afterhyperpolarization (AHP) duration 97 ms, membrane input resistance 2.2 M omega, rheobase 3.3 nA, and threshold voltage 8.1 mV). Although a portion of cells in both subpopulations of sphincter motoneurons displayed subthreshold conductances (i.e. sag, anomalous rectification), the incidence was higher in the external urethral sphincter motoneurons. The sphincter motoneuron membrane properties were likened to 'slow' hindlimb motoneurons and the low rheobase values suggest that the sphincter motoneurons are easily recruited.

A compartmental neuronal model was used to show that increased compartmental leak conductances distal to the site of excitatory postsynaptic potential (EPSP) generation have little effect on EPSP amplitude but decrease half-width markedly. Using intracellular recording from cat hindlimb motoneurons, reductions of composite Ia EPSP amplitude by up to 70% unaccompanied by reductions in half-width were seen following conditioning stimuli to hindlimb nerves. Appropriate condition-test intervals produced large reductions in EPSP amplitude that were unaccompanied by detectable increases in motoneuron conductance. These observations suggest that presynaptic inhibition and not increased postsynaptic motoneuron conductances is responsible for large EPSP amplitude reductions following conditioning stimulation.

The ability of electrical stimulation of the pontine micturition centre (PMC) to produce voiding following lumbosacral deafferentation was examined. Transection of the S3 to L7 dorsal resulted in the abolition of distension-evoked micturition while electrical stimulation of the PMC continued to produce micturition. Removal of the L7 to S2 dorsal root ganglia did not alter the PMC-evoked response, nor did transection of the dorsal roots in more rostral lumbar and thoracic segments. It appears that the PMC can activate a central neural network and produce micturition independently of lumbosacral reflex pathways.