Sensory Pudendal Nerve Research Articles

Pathways and parameters of sacral neuromodulation in rats.

The stimulation paradigm for sacral neuromodulation has remained largely unchanged since its inception. We sought to determine, in rats, whether stimulation-induced increases in bladder capacity correlated with the proportion of sensory pudendal (PudS) neurons at each stimulated location (L6, S1). If supported, this finding could guide the choice of stimulation side (left/right) and level (S2, S3, S4) in humans. Unexpectedly, we observed that acute stimulation at clinically relevant (low) amplitudes [1-1.5 × motor threshold (Tm)], did not increase bladder capacity, regardless of stimulus location (L6 or S1). More importantly for the ability to test our hypothesis, there was little anatomic variation, and S1 infrequently contributed nerve fibers to the PudS nerve. During mapping studies we noticed that large increases in PudS nerve activation occurred at amplitudes exceeding 2Tm. Thus, additional cystometric studies were conducted, this time with stimulation of the L6-S1 trunk, to examine further the relationship between stimulation amplitude and cystometric parameters. Stimulation at 1Tm to 6Tm evoked increases in bladder capacity and decreases in voiding efficiency that mirrored those produced by PudS nerve stimulation. Many animal studies involving electrical stimulation of nerves of the lower urinary tract use stimulation amplitudes that exceed those used clinically (∼1Tm). Our results confirm that high amplitudes generate immediate changes in cystometric parameters; however, the relationship to low-amplitude chronic stimulation in humans remains unclear. Additional studies are needed to understand changes that occur with chronic stimulation, how these changes relate to therapeutic outcomes, and the contribution of specific nerve fibers to these changes.NEW & NOTEWORTHY Acute low-amplitude electrical stimulation of sacral nerve (sacral neuromodulation) did not increase bladder capacity in anesthetized CD, obese-prone, or obese-resistant rats. Increasing stimulation amplitude correlated with increases in bladder capacity and pudendal sensory nerve recruitment. It is unclear how the high-amplitude acute stimulation that is commonly used in animal experiments to generate immediate effects compares mechanistically to the chronic low-amplitude stimulation used clinically.

Mapping afferent and pelvic postganglionic neurons of the urethra from female rats: The L6 DRG is the major primary afferent supplier.

To map sensory and pelvic postganglionic neurons from three different regions of the female rat urethra. The neuronal tracer True Blue (TB) was injected into the pre-pelvic, pelvic, and clitoral regions of the urethra from female Wistar rats. Seven days after TB injection, TB+ cells from the dorsal root ganglia (DRGs) and the major pelvic ganglion (MPG) were examined. The number and morphometry of TB+ cells were determined. TB+ cells were mainly distributed in lumbar 1 (L1), lumbar 2 (L2), lumbar 6 (L6), and sacral 1 (S1) DRGs, and in the MPG. The mean number of sensory neurons was 1200 ± 143. TB injection in pre-pelvic and pelvic urethra labeled neurons in L1, L2, L6, and S1 DRGs. TB injection in clitoral urethra labeled neurons in L6 and S1 DRGs. L6 DRG contained >50% of the total urethral TB+ neurons, and ~80% of the clitoral region. The mean value of the total number of MPG TB+ neurons was 1217 ± 72. DRG and MPG neurons projecting to the urethra presented a somatotopic distribution. The results demonstrated that L6 DRG is the major supplier of afferent innervation to the urethra, and that the distal urethral region is exclusively innervated by lower lumbosacral DRGs. Considering that electrical stimulation of sensory pudendal nerve improves overactive bladder, and that most of the sensory neurons in the distal urethra are from L6 DRG, electrical stimulation of this ganglion may be an innovative and effective neuromodulation therapy for neurogenic urinary dysfunctions.

Sensory pudendal nerve stimulation increases bladder capacity through sympathetic mechanisms in cyclophosphamide-induced cystitis rats.

Interstitial cystitis and bladder pain syndrome is a prevalent health concern with inadequate treatments. Neuromodulation has emerged as a therapeutic option to treat patients refractory to standard care. The objective of this study was to determine the efficacy and mechanism(s) of sensory pudendal nerve stimulation on bladder function in cystitis rats. Female rats were administered saline (n = 8) or cyclophosphamide (CYP, 150 mg/kg IP, n = 16) and single-trial cystometry experiments were conducted under urethane anesthesia 48 h after injection. Electrical stimulation (0.02-0.22 mA, 10-20 Hz) was delivered to the sensory branch of the pudendal nerve and its effect on the bladder and external urethral sphincter were measured. Stimulation trials were also conducted following bilateral hypogastric nerve transection (HGNT) or pharmacological inhibition of beta-adrenergic receptors (propranolol, 1 mg/kg IV) to determine the mechanisms of bladder inhibition. CYP-induced cystitis decreased bladder capacity (P = 0.0352) and bladder compliance (P = 0.024) by up to 38% of control. Electrical stimulation of the sensory pudendal nerve increased bladder capacity (P < 0.0001) in control and CYP rats by up to 51-52% of their respective baselines. HGNT did not influence bladder inhibition generated by sensory pudendal nerve stimulation in control rats, whereas HGNT and propranolol decreased the efficacy of electrical stimulation in CYP rats. Sympathetic reflex activity mediates sensory pudendal nerve stimulation in CYP treated but not control rats. These studies demonstrate an alternative approach to neuromodulation in cystitis and establish mechanistic changes during stimulation that may enable the development of novel therapeutics.

Stimulation of the sensory pudendal nerve increases bladder capacity in the rat.

Pudendal nerve stimulation is a promising treatment approach for lower urinary tract dysfunction, including symptoms of overactive bladder. Despite some promising clinical studies, there remain many unknowns as to how best to stimulate the pudendal nerve to maximize therapeutic efficacy. We quantified changes in bladder capacity and voiding efficiency during single-fill cystometry in response to electrical stimulation of the sensory branch of the pudendal nerve in urethane-anesthetized female Wistar rats. Increases in bladder capacity were dependent on both stimulation amplitude and rate. Stimulation that produced increases in bladder capacity also led to reductions in voiding efficiency. Also, there was a stimulation carryover effect, and increases in bladder capacity persisted during several nonstimulated trials following stimulated trials. Intravesically administered PGE2 reduced bladder capacity, producing a model of overactive bladder (OAB), and sensory pudendal nerve stimulation again increased bladder capacity but also reduced voiding efficiency. This study serves as a basis for future studies that seek to maximize the therapeutic efficacy of sensory pudendal nerve stimulation for the symptoms of OAB.

Characterization of bulbospongiosus muscle reflexes activated by urethral distension in male rats

The urethrogenital reflex (UGR) is used as a surrogate model of the autonomic and somatic nerve and muscle activity that accompanies ejaculation. The UGR is evoked by distension of the urethra and activation of penile afferents. The current study compares two methods of elevating urethral intraluminal pressure in spinalized, anesthetized male Sprague-Dawley rats (n = 60). The first method, penile extension UGR, involves extracting the penis from the foreskin, so that urethral pressure rises due to a natural anatomical flexure in the penis. The second method, penile clamping UGR, involves penile extension UGR with the addition of clamping of the glans penis. Groups of animals were prepared that either received no additional treatment, surgical shams, or received bilateral nerve cuts (4 nerve cut groups): either the pudendal sensory nerve branch (SbPN), the pelvic nerves, the hypogastric nerves, or all three nerves. Penile clamping UGR was characterized by multiple bursts, monitored by electromyography (EMG) of the bulbospongiosus muscle (BSM) accompanied by elevations in urethral pressure. The penile clamping UGR activity declined across multiple trials and eventually resulted in only a single BSM burst, indicating desensitization. In contrast, the penile extension UGR, without penile clamping, evoked only a single BSM EMG burst that showed no desensitization. Thus, the UGR is composed of two BSM patterns: an initial single burst, termed urethrobulbospongiosus (UBS) reflex and a subsequent multiple bursting pattern (termed ejaculation-like response, ELR) that was only induced with penile clamping urethral occlusion. Transection of the SbPN eliminated the ELR in the penile clamping model, but the single UBS reflex remained in both the clamping and extension models. Pelvic nerve (PelN) transection increased the threshold for inducing BSM activation with both methods of occlusion but actually unmasked an ELR in the penile extension method. Hypogastric nerve (HgN) cuts did not significantly alter any parameter. Transection of all three nerves eliminated BSM activation completely. In conclusion, penile clamping occlusion recruits penile and urethral primary afferent fibers that are necessary for an ELR. Urethral distension without significant penile afferent activation recruits urethral primary afferent fibers carried in either the pelvic or pudendal nerve that are necessary for the single-burst UBS reflex.

Pudendal neuromodulation improves voiding efficiency in diabetic rats

Diabetic cystopathy is typically manifested as bladder voiding dysfunction, and numerous patients are refractory to standard therapy. In this study, we determined whether electrical stimulation (ES) of the sensory branch of the pudendal nerve could engage an augmenting reflex and thereby improve bladder emptying in a diabetic animal model with cystopathy. The efficiency of bladder emptying with ES of the sensory branch of the pudendal nerve at different stimulation intensities was measured in rats at 8 or 18 weeks after the induction of diabetes with streptozotocin. The voiding efficiency (VE) was reduced from 74 ± 4% to 30 ± 8% in rats with diabetes for 8 weeks and from 73 ± 6% to 20 ± 6% in rats with diabetes for 18 weeks. ES at lower intensities (0.025-0.05 mA) applied to the pudendal sensory nerve did not affect the VE in rats with diabetes for 18 weeks but increased the VE in rats with diabetes for 8 weeks. Subsequently, when the stimulation intensity was elevated to 0.1-0.3 mA, the VEs in rats with diabetes for both 8 and 18 weeks increased to 40-50%. The results of the present study are consistent with the essential role for pudendal sensory feedback in efficient bladder emptying, and electrical activation of the sensory branch of the pudendal nerve was efficient restoring the voiding function in diabetic animals with cystopathy. This could provide an approach to improve bladder emptying in diabetic patients with voiding dysfunction.

Sacro-lumbar Intersegmental Spinal Reflex in Autonomic Pathways Mediating Female Sexual Function

Autonomic neurons in paracervical ganglia mediating vasodilation in the female reproductive tract receive inputs from both midlumbar and sacral spinal levels. However, it is not known how the lumbar pathways are activated. This study tested whether stimulation of pudendal sensory nerve could activate lumbar spinal outflows to paracervical ganglia via a spinal reflex pathway. Isolated spinal cords with attached peripheral nerves were removed from urethane-anesthetized female guinea pigs and perfused via the aorta with physiological salt solution. Spinal pathways to midlumbar preganglionic neurons were tested by recording extracellular compound action potentials (CAPs) in lumbar splanchnic or distal hypogastric nerves after electrical stimulation of thoracic spinal cord or the pudendal nerve. CAPs also were recorded from pelvic nerves after pudendal nerve stimulation. Sensory neurons were retrogradely traced from the pudendal nerve and characterized immunohistochemically. Activation of preganglionic neurons projecting from midlumbar spinal cord to paracervical ganglia following stimulation of pudendal sensory nerves in isolated preparations. Thoracic spinal cord stimulation produced CAPs in hypogastric nerves that were abolished by transection of L3 lumbar splanchnic nerves. Pudendal nerve stimulation produced CAPs in L3 lumbar splanchnic, hypogastric, and pelvic nerves, demonstrating an ascending intersegmental spinal circuit to midlumbar levels in addition to the sacral spinal circuit. These CAPs in hypogastric nerves were enhanced by bicuculline (10 µM), blocked by tetrodotoxin (1 µM) but were not affected by hexamethonium (200 µM). Retrograde axonal tracing revealed four groups of sensory neurons in S3 dorsal root ganglia that were distinguished immunohistochemically. Midlumbar preganglionic neurons projecting to paracervical ganglia regulating blood flow and motility in the female reproductive tract can be activated by an ascending intersegmental spinal pathway from pudendal sacral inputs, which is inhibited by local spinal circuits. This pathway will help understand pathological conditions affecting reproductive function.

Functional Coupling Between Motor and Sensory Nerves Through Contraction of Sphincters in the Pudendal Area of the Female Cat

The question of whether skin receptors might help in the perception of muscle contraction and body movement has not been settled. The present study gives direct evidence of skin receptor firing in close coincidence with the contraction of the vaginal and anal sphincters. The distal stump of the sectioned motor pudendal nerve was stimulated. Single shocks induced a wavelike increase in the lumen pressure of the distal vagina and the anal canal, as well as constriction of the vaginal introitus and the anus. The constriction pulls on and moves the surrounding skin, which was initially detected visually. In the present experiments, a thin strain gauge that pressed on the skin surface detected its displacement. Single shocks to the motor nerve induced a wave of skin movement with maximal amplitude at 5 mm from the anus and propagated with decrement beyond 35 mm. The peripheral terminals of the sensory pudendal nerve and the posterior femoral nerve supply the skin that moves. Sensory axons from both nerves fired in response to both tactile stimulation and the skin movement produced by the constriction of the orifices (motor-sensory coupling). In cats with all nerves intact, a single shock to the sensory nerves induced reflex waves of skin movement and lumen pressure (sensory-motor coupling). Both couplings provide evidence for a feedforward action that might help to maintain the female posture during mating and to the perception of muscle contraction.

Activation of Somatosensory Afferents Elicit Changes in Vaginal Blood Flow and the Urethrogenital Reflex Via Autonomic Efferents

We examined the effects of pudendal sensory nerve stimulation and urethral distention on vaginal blood flow and the urethrogenital reflex, and the relationship between somatic and autonomic pathways regulating sexual responses. Distention of the urethra and stimulation of the pudendal sensory nerve were used to evoke changes in vaginal blood flow (laser Doppler perfusion monitoring) and pudendal motor nerve activity in anesthetized, spinally transected female rats. Bilateral cuts of either the pelvic or hypogastric nerve or both autonomic nerves were made, and blood flow and pudendal nerve responses were reexamined. Stimulation of the pudendal sensory nerve or urethral distention elicited consistent increases in vaginal blood flow and rhythmic firing of the pudendal motor nerve. Bilateral cuts of the pelvic plus hypogastric nerves significantly reduced vaginal blood flow responses without altering pudendal motor nerve responses. Pelvic nerve cuts also significantly reduced vaginal blood flow responses. In contrast, hypogastric nerve cuts did not significantly change vaginal blood flow. Bilateral cuts of the pudendal sensory nerve blocked pudendal motor nerve responses but stimulation of the central end evoked vaginal blood flow and pudendal motor nerve responses. Stimulation of the sensory branch of the pudendal nerve elicits vasodilatation of the vagina. The likely mechanism is via activation of spinal pathways that in turn activate pelvic nerve efferents to produced changes in vaginal blood flow. Climatic-like responses (firing of the pudendal motor nerve) occur in response to stimulation of the pudendal sensory nerve and do not require intact pelvic or hypogastric nerves.

Improved bladder emptying in urinary retention by electrical stimulation of pudendal afferents

Urinary retention is the inability to empty the bladder completely, and may result from bladder hypocontractility, increases in outlet resistance or both. Chronic urinary retention can lead to several urological complications and is often refractory to pharmacologic, behavioral and surgical treatments. We sought to determine whether electrical stimulation of sensory fibers in the pudendal nerve could engage an augmenting reflex and thereby improve bladder emptying in an animal model of urinary retention. We measured the efficiency of bladder emptying with and without concomitant electrical stimulation of pudendal nerve afferents in urethane-anesthetized rats. Voiding efficiency (VE = voided volume/initial volume) was reduced from 72 ± 7% to 29 ± 7% following unilateral transection of the sensory branch of the pudendal nerve (UST) and from 70 ± 5% to 18 ± 4% following bilateral transection (BST). Unilateral electrical stimulation of the proximal transected sensory pudendal nerve during distention-evoked voiding contractions significantly improved VE. Low-intensity stimulation at frequencies of 1–50 Hz increased VE to 40–51% following UST and to 39–49% following BST, while high-intensity stimulation was ineffective at increasing VE. The increase in VE was mediated by increases in the duration of distention-evoked voiding bladder contractions, rather than increases in contraction amplitude. These results are consistent with an essential role for pudendal sensory feedback in efficient bladder emptying, and raise the possibility that electrical activation of pudendal nerve afferents may provide a new approach to restore efficient bladder emptying in persons with urinary retention.

Spinal neurons activated in response to pudendal or pelvic nerve stimulation in female rats

The overlapping distribution of spinal neurons activated with either pudendal sensory nerve or pelvic nerve stimulation was examined in the female rat using c-fos immunohistochemistry. Pudendal sensory nerve stimulation resulted in a significant increase in fos-positive cells in the ipsilateral dorsal horn and bilaterally in the medial, lateral and intermediate gray of L5-S1. Pelvic nerve stimulation resulted in significant increases of c-fos immunoreactive nuclei in the ipsilateral dorsal horn, lateral and intermediate gray and bilaterally in the medial gray of L5-S1. Co-distribution of fos immunoreactive nuclei with the vesicular glutamate transporters (VGlut2 and VGlut3) and neurokinin I receptors were found in distinct regions of the dorsal horn, medial and lateral gray. Specific areas in the medial dorsal horn, dorsal gray commissure, laminae VI and X and dorsal lateral gray were activated after stimulation of the pudendal sensory and pelvic nerves, suggesting these areas contain spinal neurons that receive both somatomotor and visceral inputs and are part of the intraspinal circuit that regulates sexual and voiding function.

Pudendal nerve stimulation, interneurons post-discharge and delayed depolarization in hind limb motoneurons of the female cat

The present experiments were done in the spinal female cat. In a prior work in the decerebrate female cat, stimulation of the sensory pudendal nerve (SPN) induced a depolarizing wave (LD) in hind limb motoneurons that outlasted the stimulus by up to 6 s. LD triggered self-sustained motoneuron firing (bistability). An intrinsic potential underlies bistable firing, which, in the cat, depends on two main factors; first, the integrity of pathways descending from the brain stem to the spinal cord and, second, the membrane potential of the motoneuron just before the stimulus; at high resting potential, excitatory short-lasting inputs induce transient but no sustained firing. Thus, no bistability occurs in the spinal cat or in hyperpolarized motoneurons of the decerebrate cat. LD might be an intrinsic potential that could also be absent in the spinal cat, or an extrinsic (synaptic) potential induced by spinal interneurons. In the latter case, the interneurons generating LD should show post-discharge as prolonged as LD. LD was produced in spinal cats and its amplitude did not change or increase slightly during hyperpolarizing pulses, which suggests that LD might be a synaptic response. Interneurons showing post-discharge to train of stimulation to SPN were located 100–200 μm above the pools of hind limb motoneurons. Some post-discharges were as prolonged as LD. We conclude that LD might be a synaptic response to local interneurons.

Spinal neurons activated with the urethrogenital reflex in the male rat

The urethrogenital (UG) reflex is a spinal ejaculatory-like reflex. The location of spinal neurons activated by the UG reflex was examined in the male rat using the immediate early gene, c- fos. In addition, co localization of neurons containing galanin and choline acetyl transferase (ChAT) and serotonin fibers with fos-immunoreactive (fos-I) nuclei was examined. Activation of the UG reflex resulted in a significant increase in fos positive nuclei in segments T13–S1, compared to controls in which the UG reflex was not activated. Spinal circuits involved in the UG reflex include neurons relaying afferent information from the pudendal sensory nerve, in the dorsal horn and medial cord of L5–S1. Interneurons specifically activated with the UG reflex were identified in the medial, intermediate and lateral gray. A small proportion of parasympathetic and sympathetic preganglionic neurons in the intermediolateral cell column (IML) of L5–S1 and IML and medial gray of T13–L2, respectively, was activated with the UG reflex. A significant increase in the number of galanin containing neurons expressing c- fos in the medial gray of L3–L4 was also observed with the UG reflex. Serotonin fibers and varicosities were found throughout the spinal cord and were especially dense in the ventral horn, IML and medial gray. Fos activated neurons were found in close apposition to serotonin fibers in the IML and medial gray. These studies demonstrate the multisegmental intraspinal circuitry responsible for ejaculatory-like responses and demonstrate the potential involvement of galanin, acetylcholine and serotonin in mediation of the UG reflex.

Gamma->alpha linkage and persistent firing of Ia fibers by pudendal nerve stimulation in the decerebrate cat.

The sensory pudendal nerve (SPN) was stimulated in decerebrate female cats. Spikes of single Ia muscle spindle afferents from the medial gastrocnemius (MG) muscle were recorded in dorsal root filaments. Electroneurography (ENG) was recorded in a cut nerve filament to the MG muscle; MG electromyography (EMG) was also recorded. Single shock to SPN induced discharges of small ENG spikes (SS) with similar amplitude to that of gamma spikes elicited by ventral root stimulation. Thus SS were identified as gamma spikes. The latency of the gamma discharge was approximately 15 ms. As expected, the onset of the gamma discharge preceded a discharge of Ia spikes; the time difference between both discharges was approximately 5 ms. After the initial bursts, the Ia and the gamma activities paused during 20-30 ms but later increased again to last approximately 1 s. After the shock, the EMG activity was depressed during approximately 50 ms; later, motor-unit spikes may show transient activation. Thus the onset of the gamma activation preceded the activation of motor units (gamma-->alpha link). Trains of shocks (1 or 100 Hz) to SPN induced a sustained increase in the frequency of gamma spikes, Ia spikes, and motor units that outlasted the train by 20-120 s. The sustained firing of Ia fibers might trigger or help to trigger and maintain the response of alpha-motoneurons.

Identification of spinal neurons involved in the urethrogenital reflex in the female rat.

The urethrogenital (UG) reflex is a spinal sexual reflex that consists of autonomic and somatic nerve activity and vaginal, uterine, and anal sphincter contractions. The UG reflex is under tonic descending inhibition by neurons in the region of the nucleus paragigantocellularis (nPGi). The location of spinal neurons activated by the UG reflex was examined in the female rat using the immediate early gene, c-fos. In addition, the descending inputs from the nPGi onto fos-activated neurons was examined using the anterograde tracer biotin dextran amine injected into the nPGi. The UG reflex resulted in a significant increase in fos-positive nuclei in segments T12-S1, compared with experimental controls in which the UG reflex was not activated. Spinal circuits involved in the UG reflex include neurons relaying afferent information from the pudendal sensory nerve, in the dorsal horn and medial cord of L5-S1. Efferent output includes preganglionic neurons located in the lateral gray of L5-S1 and lateral and medial gray of T13-L2. Spinal interneurons involved in the UG reflex were found close to the preganglionic neurons and in the dorsal horn and intermediate and medial gray of T12-S1. NPGi inputs were found primarily on the autonomic efferents and interneurons in the medial and intermediate gray. These studies demonstrate multisegmental spinal circuits activated with the UG reflex and demonstrate that the descending inhibition from the nPGi is by means of preganglionic and somatic efferents and spinal interneurons closely associated with the efferent output.

Sustained firing of alpha and gamma hind limb motoneurons induced by stimulation of the pudendal nerve.

Axons from receptors in the cat vaginal wall run in the sensory pudendal nerve (SPN), and brief (<10 s) vaginal probing (VP) in the decerebrate cat produces a long-lasting (>1 min) contraction of the triceps surae (TS) muscles. The aim of the present project was to find out whether brief SPN stimulation also produces sustained TS response and, eventually, to study the mechanisms involved in it. Decerebrate female cats were used. In some cats, TS electromyography (EMG) and tension response were recorded; stimulation of left SPN with single or repetitive trains of shocks produced a bilateral TS response that outlasted the stimulus >1 min as VP did. In paralyzed cats (pancuronium; Panc), intracellular recordings were made from hind limb motoneurons (MNs). SPN stimulation produced a depolarization <or=5 s long and occasional cell firing only lasting <2.5 s; this is in contrast with the prolonged TS postdischarge seen in nonparalyzed cats. If MNs were depolarized below the firing threshold by current injection, about half of them showed bistable firing that could last several minutes in response to SPN train. It is suggested that MNs might hyperpolarize after Panc injection. Before Panc injection, SPN train produced long-lasting (>1 min) electroneurographic (ENG) postdischarge in a small filament of the medial gastrocnemius (MG) nerve; the MG EMG postdischarge was also recorded. Large spikes (LS) and small spikes (SS) were distinguished in the ENG. During the postdischarge, LS frequency and the integrated EMG activity correlated well (r > 0.9); no correlation was found between SS and EMG. After Panc injection, LS postdischarge was absent but the SS postdischarge remained. LS followed by EMG potential were also evoked by brief TS stretch (reflex LS); single shocks to SPN only elicited SS that were not followed by EMG potential. It is concluded that alpha axons and gamma axons produced LS and SS, respectively, and that SPN activates gamma axons. It is proposed that, in the nonparalyzed cats, the stimulation of SPN with trains of shocks might cause an increase in the afferent inflow from muscle spindles to alpha MNs through the sustained firing of gamma MNs. The increased excitatory inflow would depolarize alpha MNs and allow bistable MN firing; Panc would decrease this inflow by blocking transmission to the spindle fibers.

Urethral pudendal afferent-evoked bladder and sphincter reflexes in decerebrate and acute spinal cats

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.

Pelvic and pudendal reflexes in the in vitro neonatal rat preparation

Pudendal-to-pelvic and pudendal-to-pudendal reflexes are described in an in vitro brainstem-spinal cord neonatal rat preparation. Cytometrograms and peripheral pelvic nerve recordings were used to monitor excitatory micturition reflexes evoked by tactile perineal stimulation or by continuous electrical stimulation of the sensory pudendal nerve. Micturition was characterized by an increased bladder pressure and a period of tonic pelvic nerve activity during which time fluid was expelled from the urethra. Single stimuli delivered to the sensory pudendal nerve evoked a phasic response in the pelvic nerve (pudendal-to-pelvic reflex) or pudendal motor nerve (pudendal-to-pudendal reflexes). The pudendal-to-pelvic reflex consisted of a single response occurring after a mean latency of 98 ± 24 ms. The pudendal-to-pudendal reflex was comprised of two responses, the first occurred at a mean latency of 105 ± 11 ms and the second at 383 ± 36 ms. Cervical or lower thoracic spinal transection did not alter the pudendal-to-pelvic reflex, however, the second component of the pudendal-to-pudendal reflex was abolished. The use of preganglionic pelvic and pudendal peripheral nerve recordings described in this study provide a direct measure of the reflex outflow from the CNS and can be used to examine developmental changes and neurochemical substrates within the CNS which contribute to micturition and coital reflexes in the rat.

Androgenic modulation of the activity of lumbar neurons involved in the rat bulbocavernosus reflex.

The bulbocavernosus (BC) reflex, produced in the BC motor nerve in response to electrical stimulation of the contralateral pudendal sensory nerve, was investigated in intact, castrated, and testosterone-treated castrated male rats under urethane anesthesia. No significant group differences in the reflex latency, sensory or motor conduction velocity, or central delay were observed. A conditioning pulse to the pudendal sensory nerve caused suppression of the averaged antidromic field potential recorded in the contralateral spinal nucleus of the bulbocavernosus (SNB) after stimulation of the SNB axons in the BC motor nerve. The suppression occurred at 6- to 35-ms intervals between shocks to pudendal sensory nerve and BC motor nerve, and was markedly smaller in castrated males than in the other two groups. In contrast, a conditioning pulse to the contralateral BC motor nerve had no effect on the SNB antidromic field potential. These results indicate that androgen modulates the efficacy of synaptic transmission onto SNB motoneurons or other neurons involved in the BC reflex.

Spinal distribution of extracellular field potentials generated by electrical stimulation of pudendal and perineal afferents in the cat.

Electrical stimulation of sensory pudendal and superficial perineal nerves evokes focal synaptic potentials produced by activation of spinal neurons in the lumbosacral gray matter in chloralose anesthetized or decerebrate cats. The field potentials evoked by sensory pudendal nerve stimulation were located in medial parts of laminae V and VI, and lamina X in the S1 to S3 spinal segments. The superficial perineal cutaneous field potentials partially overlapped with those produced by the pudendal nerve, but in general were localized more laterally in laminae V and VI. The central latencies of the earliest portion of the field potentials evoked by either sensory pudendal or superficial perineal nerves were less than 0.9 ms suggesting that monosynaptic activation of neurons contributed to the potentials.