Neural control of the lower urinary tract.
Explore the source record for details and available documents.
Afferent Pathways↗
Biomedical subjects
W C de Groat
Publications and source records attributed to W C de Groat.
Detrusor-sphincter dyssynergia induced by cold stimulation of the urinary bladder of rats.
Instillation of cold water into the urinary bladder has been used as a diagnostic test to evaluate neurogenic dysfunctions of the lower urinary tract (LUT). This study examined the effects of cold stimulation on the LUT of urethan-anesthetized rats. Urinary bladder pressure and external urethral sphincter (EUS) electromyogram (EMG) were recorded during cystometrograms in which body- or room-temperature saline was infused continuously into the bladder and voided through the urethra. Subsequent infusion of cold saline (6-8 degrees C) into the bladder increased by approximately 100% the duration and amplitude of supraspinal reflex bladder contractions, increased baseline bladder pressure, increased the pressure threshold for inducing micturition, and increased EUS EMG activity. Blocking EUS activity by transecting the pudendal nerves or by administering a neuromuscular blocking agent markedly reduced or eliminated the effect of cold stimulation. Capsaicin pretreatment suppressed the effect of cold stimulation. It is concluded that cold temperatures stimulate capsaicin-sensitive C fiber bladder afferents that reflexly activate the EUS, producing detrusor and sphincter dyssynergia and increasing urethral outlet resistance. This in turn increases the amplitude and duration of bladder contractions during voiding.
Acclimatization↗
Influence of anesthesia on bladder hyperactivity induced by middle cerebral artery occlusion in the rat.
The effect of anesthesia or an N-methyl-D-aspartate (NMDA) glutamatergic antagonist (MK-801) on bladder hyperactivity induced by unilateral middle cerebral artery (MCA) occlusion was examined in female rats. Before infarction, control bladder contractions were monitored in two groups of rats: 1) awake and 2) urethan anesthetized. The awake rats were then anesthetized with halothane, and MCA occlusion was performed in both groups. After recovery from halothane, bladder capacity in awake rats was significantly reduced (60.8 +/- 1.3%) 0.5-4.5 h after MCA occlusion but not changed in urethan-anesthetized rats. MK-801 (0.1 mg/kg i.v.) administered before MCA occlusion blocked the reduction in bladder capacity in awake rats 1.5-4.5 h after MCA occlusion. Bladder capacity was not changed by sham operation in either the awake or urethan-anesthetized rats. Urethan administered after recovery from halothane anesthesia increased bladder capacity in MCA-occluded awake rats but not in sham-operated awake rats. Infarct areas in halothane, urethan-anesthetized, or MK-801-treated rats were not significantly different. These results indicate that cerebral infarction induces bladder hyperactivity in awake rats and that urethan or MK-801 inhibits the development of this hyperactivity, most likely by blocking glutamatergic transmission in the brain.
Anesthesia, Inhalation↗
Modification of urinary bladder function after spinal cord injury.
Explore the source record for details and available documents.
Humans↗
Effects of LY215490, a competitive alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor antagonist, on the micturition reflex in the rat.
The effects of glutamate receptor antagonists on urinary bladder and external urethral sphincter- (EUS) electromyogram (EMG) activity were evaluated in unanesthetized decerebrate rats. In normal rats, LY215490, an alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor antagonist, in small i.v. doses (1-3 mg/kg) decreased bladder contraction amplitude (BC-Amp) by 29% and EUS-EMG by 41%; whereas a large dose (10 mg/kg) completely abolished bladder and EUS-EMG activity. LY215490 injected intrathecally in small doses (0.01-0.1 microg) decreased BC-Amp by 20% and EUS-EMG by 62%; whereas large doses (1-10 microg) completely abolished bladder and EUS-EMG activity. LY215490 (0.1 microg i.t.) increased bladder capacity by 28% and decreased voiding efficiency by 44%. Combined i.t. administration of small doses of LY215490 (0.1 microg) and MK-801 (1 microg), an N-methyl-D-aspartate (NMDA) receptor antagonist, which individually had little effect on BC-Amp, markedly suppressed bladder activity. In chronic spinal rats, LY215490 (10 mg/kg i.v.) abolished EUS-EMG activity and decreased BC-Amp by 41%. Intrathecal injections of LY215490 were also less effective in chronic spinal rats; a 10-microg dose producing only a partial block (53%) of BC-Amp, but complete block of EUS-EMG. In chronic spinal rats, MK-801 (1 mg/kg i.v.) abolished EUS-EMG activity and decreased BC-Amp by 36%. Pretreatment with MK-801 (1 mg/kg i.v.) did not enhance the effect of LY215490 on bladder activity in chronic spinal rats. These data suggest that AMPA glutamate receptors have a major role in the excitatory pathways controlling bladder and EUS activity in spinal cord intact rats. However, in chronic spinal rats, AMPA and NMDA receptors are essential for EUS reflexes, but are responsible for only a part of reflex bladder activity.
Animals↗
Reorganization of somato-urethral reflexes following spinal cord injury in the rat.
PURPOSE: It is known that reflex activity of the urinary bladder can be inhibited or facilitated by perineal cutaneous stimulation. This study was undertaken to examine the urethral striated (EUS) and smooth muscle responses evoked by perineal cutaneous stimulation in the rat. MATERIALS AND METHODS: Urethral perfusion pressure and EUS-EMG were monitored in urethane-anesthetized normal and chronic spinal rats (4-5 weeks after T(8-9) spinalization) of either sex. Somatic perineal stimulation was performed by tactile or pinch stimulation to the perineum. RESULTS: In both normal and chronic spinal rats, perineal stimulation elicited a transient increase in EUS-EMG activity which was abolished following neuromuscular blockade with alpha-bungarotoxin i.v. In normal rats treated with alpha-bungarotoxin perineal stimulation did not elicit a detectable urethral smooth muscle response. However, in chronic spinal rats perineal stimulation increased urethral pressure by smooth muscle contraction in males and decreased urethral pressure by smooth muscle relaxation in females. The evoked urethral smooth muscle contraction in males was significantly reduced or abolished by atropine i.v., but not by sympathetic nerve transection or prazosin i.v., whereas the relaxation in females was significantly reduced or abolished by N-nitro-L-arginine methyl ester (a nitric oxide synthase inhibitor, i.v.). CONCLUSIONS: These data indicate that spinal cord injury unmasks somato-urethral smooth muscle reflexes mediated by lumbosacral parasympathetic efferent pathways. The reflexes consist of a nitric oxide-mediated urethral relaxation in females and an atropine-sensitive urethral contraction in male rats.
Animals↗
Corticotropin releasing factor-like immunoreactivity in afferent projections to the sacral spinal cord of the cat.
Distribution and origin of corticotropin releasing factor (CRF) in the thoraco-lumbar and sacral spinal cord of the cat has been studied using immunohistochemical method. CRF immunoreactive (CRF-IR) nerve fibers and terminals were most prominent in dorsal part of sacral spinal cord. In the sacral segments of the spinal cord, immunoreactivity for CRF was detected in a prominent bundle of axons and varicosities extending from Lissauer's tract (LT) along the lateral edge of the superficial dorsal horn (laminae I and II) to laminae V at the base of the dorsal horn. Individual CRF-IR fibers passed from the bundle in ventral medial and ventrolateral directions to the dorsal commissure and the sacral preganglionic nucleus (SPN), respectively. The bundle of CRF-IR axons closely resembled vasoactive intestinal polypeptide (VIP) containing fibers in LT and on the lateral edge of the dorsal horn. Sacral dorsal root transection eliminated both the CRF and VIP fiber staining in the dorsal horn. Spinal transection at the T12-T13 segmental level did not influence the CRF- or VIP-IR. Less intense CRF-IR was also present in fibers in: (1) the dorsal lateral funiculus adjacent to LT, (2) the superficial layers of the dorsal horn and intermediolateral nucleus at thoracolumbar spinal levels, (3) the ventral horn, including Onuf's nucleus, (4) the intermediate gray matter including the dorsal gray commissure, and (5) the SPN. The similarity in the distribution of CRF-IR and pelvic nerve afferent projections in the sacral spinal cord raises the possibility that CRF may be a transmitter in afferent neurons innervating the pelvic viscera.
Animals↗
M1 muscarinic receptor-induced facilitation of ACh and noradrenaline release in the rat bladder is mediated by protein kinase C.
1. [3H]Noradrenaline (NA) AND [14C]acetylcholine (ACh) released by electrical field stimulation were measured simultaneously in strips from the body of rat urinary bladder. 2. [3H]NA and [14C]ACh release was greater during continuous stimulation (CS; 10 Hz, 100 shocks) or in the presence of eserine than during intermittent train stimulation (IS; 10 Hz, 10 shocks every 5 s, 10 times). Atropine (1 microM) or pirenzepine (0.05-0.1 microM) blocked the CS- or eserine-facilitated release. 3. The protein kinase C (PKC) activator phorbol dibutyrate (PDB; 0.05 and 0.5 microM) increased the release of both [3H]NA and [14C]ACh in a concentration-dependent manner. Atropine blocked the PDB-induced facilitation of ACh release but not the facilitation of NA release. 4. The protein kinase A (PKA) activator 8-Br-cAMP did not affect ACh release but enhanced NA release. 5. The PKC inhibitor H-7 (50-100 microM) inhibited the CS- or eserine-facilitated release of both ACh and NA, but did not affect the non-facilitated release evoked by IS. H-7 also inhibited 0.5 microM PDB-induced facilitation of ACh release but not NA release. 6. Down-regulating PKC by pretreatment for 30 min with 5 microM PDB decreased the facilitated release of ACh and the eserine-induced facilitation of NA release. 7. Electrically evoked contractions of the bladder strips exhibited a biphasic response to PDB (2.5 microM), which consisted of an initial enhancement of the peak amplitude and area followed after 20 min by an inhibition of contractions. H-7 inhibited the electrically evoked contractions in a dose-dependent fashion. 8. It is concluded that a phospholipase C-PKC signal transduction pathway is essential for muscarinic receptor-induced facilitation of ACh and NA release but is not involved in the non-facilitated release of transmitters in the rat urinary bladder.
Acetylcholine↗
Different types of Na+ and A-type K+ currents in dorsal root ganglion neurones innervating the rat urinary bladder.
1. Whole-cell patch-clamp recording in combination with axonal tracing techniques was used to examine the electrical properties of afferent neurones innervating the urinary bladder of the adult rat. Individual bladder afferent cells were labelled by Fast Blue (FB), injected into the bladder wall. 2. Passive and active electrical parameters at room temperature (20-22 degrees C) in FB-labelled bladder afferent neurones were comparable with those in unlabelled neurones. Unselected dorsal root ganglion (DRG) neurones as well as bladder afferent neurones exhibited two different types of action potential: high-threshold humped spikes in small-sized neurones and low-threshold narrow spikes in large-sized neurones. 3. The majority (70%) of bladder neurones which were small in size expressed high-threshold tetrodotoxin (TTX)-resistant Na+ channels and slow-inactivating A-type K+ channels (KA), which were available at the resting membrane potential, whereas large-sized DRG neurones had low-threshold TTX-sensitive Na+ channels and fast-inactivating KA channels, which were almost completely inactivated at the resting membrane potential. 4. Half-maximal conductances of activation of TTX-resistant and TTX-sensitive Na+ currents were obtained at -10.3 and -25.3 mV, respectively. The TTX-resistant and TTX-sensitive Na+ currents were half-inactivated at -25.3 and -56 mV, respectively. 5. In the TTX-resistant neurones, the transient outward K+ current (A-type current, IA) with half-maximal conductance at -40.8 mV was half-inactivated at -77.5 mV, and exhibited slower decaying kinetics (mean decay constant (tau), 240 ms) than the IA current recorded from the large-sized TTX-sensitive neurones (mean tau, 20 ms). 6. These results suggest that the majority of bladder afferent neurones have high electrical thresholds for spike activation due to the TTX-resistant Na+ current and the slow-inactivating IA current, which reflect the large population of unmyelinated high-threshold C fibre afferents that innervate the urinary bladder.
Action Potentials↗
Increased expression of neuronal nitric oxide synthase in bladder afferent pathways following chronic bladder irritation.
Immunocytochemical techniques were used to examine alterations in the expression of neuronal nitric oxide synthase (NOS) in bladder pathways following acute and chronic irritation of the urinary tract of the rat. Chemical cystitis was induced by cyclophosphamide (CYP) which is metabolized to acrolein, an irritant eliminated in the urine. Injection of CYP (n = 10, 75 mg/kg, i.p.) 2 hours prior to perfusion (acute treatment) of the animals increased Fos-immunoreactivity (IR) in neurons in the dorsal commissure, dorsal horn, and autonomic regions of spinal segments (L1-L2 and L6-S1) which receive afferent inputs from the bladder, urethra, and ureter. Fos-IR in the spinal cord was not changed in rats receiving chronic CYP treatment (n = 15, 75 mg/kg, i.p., every 3rd day for 2 weeks). In control animals and in animals treated acutely with CYP, only small numbers of NOS-IR cells (0.5-0.7 cell profiles/sections) were detected in the L6-S1 dorsal root ganglia (DRG). Chronic CYP administration significantly (P < or = .002) increased bladder weight by 60% and increased (7- to 11-fold) the numbers of NOS-immunoreactive (IR) afferent neurons in the L6-S1 DRG. A small increase (1.5-fold) also occurred in the L1 DRG, but no change was detected in the L2 and L5 DRG. Bladder afferent cells in the L6-S1 DRG labeled by Fluorogold (40 microliters) injected into the bladder wall did not exhibit NOS-IR in control animals; however, following chronic CYP administration, a significant percentage of bladder afferent neurons were NOS-IR: L6 (19.8 +/- 4.6%) and S1 (25.3 +/- 2.9%). These results indicate that neuronal gene expression in visceral sensory pathways can be upregulated by chemical irritation of afferent receptors in the urinary tract and/or that pathological changes in the urinary tract can initiate chemical signals that alter the chemical properties of visceral afferent neurons.
Acrolein↗
Increased c-fos expression in spinal neurons induced by electrical stimulation of the ureter in the rat.
The spinal processing of afferent input from the ureter was examined using an immunocytochemical technique to detect the expression of c-fos, an immediate early gene. Proximal and distal sites in one ureter were electrically stimulated separately or together at intensities that elicited a pseudo-affective response (an increase in arterial pressure). Very few Fos+ cells (range: 0.6-6.6 cells/half section were present in the L(1)-L(2), L(5)-S(2) spinal segments in sham operated control animals; however, following stimulation of the ureter, a significant increase in the numbers of Fos+ cells was detected at spinal levels L(1)-L(2) (mean 24.5-33.1 cells/half section) and L(6)-S(1) (mean 17.4-33.0 cells/half section). In L(6)-S(1), the numbers of Fos+ cells were significantly greater ipsilateral (mean 25.2 cells/half section) vs. contralateral (12.3 cells/half section) to stimulation; whereas in L(1)-L(2), the numbers were similar on both sides of the spinal cord. In L(1)-L(2), a greater percentage of Fos+ cells was present in superficial medial (MDH, 49.7%) and lateral dorsal horn (LDH, 40.8%); whereas in L(6)-S(1), the cells were more numerous in sacral parasympathetic nucleus (SPN, 38.7%) and LDH (25.6%*) regions. This distribution of Fos+ cells varies in a number of respects from that noted in previous experiments after chemical irritation of the urinary bladder and urethra which activated neurons only in L(6)-S(1) and primarily in the DCM and MDH. The results indicate that nociceptive afferent inputs from different areas of the urinary tract are processed in different regions of the spinal cord.
Animals↗
Role of NMDA and AMPA glutamatergic transmission in spinal c-fos expression after urinary tract irritation.
Chemical irritation of the lower urinary tract (LUT) of the rat increases the expression of the immediate early gene c-fos within neurons in the dorsal horn (DH), dorsal commissure (DCM), and intermediolateral region, including sacral parasympathetic nucleus (SPN) of the spinal cord (L6-S1). A previous study indicated the involvement of the N-methyl-D-aspartic acid (NMDA) receptor in this c-fos expression after LUT irritation. The role of glutamatergic synapses was further investigated using a selective and competitive alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor antagonist (LY-215490). Systemic administration of LY-215490 produced a dose-dependent decrease in the number of Fos-positive cells after LUT irritation in the DCM and SPN areas, whereas in the DH only the highest dose (10 mg/kg) of LY-215490 decreased the number of Fos-positive cells. A low dose (1 mg/kg) of either MK-801 (an NMDA antagonist) or LY-215490 alone did not alter c-fos expression. However, a combined administration of low doses of MK-801 and LY-215490 significantly decreased the number of Fos-positive cells in all regions of the spinal cord. These results indicate that AMPA as well as NMDA receptors are involved in the spinal processing of nociceptive input from the LUT and that these glutamatergic receptors play a synergistic role in visceral nociceptive processing.
Animals↗
Reorganization of the innervation of the vas deferens after sympathetic decentralization.
Reorganization of autonomic efferent pathways to the rat vas deferens was noted after chronic (30 days) sympathetic decentralization produced by hypogastric nerve (HGN) transection. In normal rats, electrical stimulation of the HGN elicited an increase in vasal pressure (VP) bilaterally, whereas pelvic nerve (PN) stimulation did not alter VP. However, after unilateral HGN transection, stimulation of the PN on the transected side but not on the normal side increased VP. The decentralized vas exhibited larger VP responses to stimulation of the contralateral HGN in comparison with the normal vas. After bilateral HGN transection, PN-induced VP responses were elicited at lower stimulus intensities than in rats with unilateral transections. PN-induced VP responses were blocked by hexamethonium and prazosin but were not altered by atropine. Distension of the vas lumen occurred after decentralization. PN-induced VP responses were not detectable in extremely distended vas. These data indicate that, after degeneration of sympathetic preganglionic axons, decentralized adrenergic ganglion cells are reinnervated by parasympathetic or sympathetic preganglionic pathways and that the reinnervation influences vasal function.
Animals↗
Role of spinal nitric oxide in the facilitation of the micturition reflex by bladder irritation.
PURPOSE: Nitric oxide (NO) is known to have an important transmitter function at peripheral synapses in the urogenital tract and has also been implicated in the transmission of nociceptive information in the spinal cord. The present study evaluated the role of NO in the central micturition reflex pathway. MATERIALS AND METHODS: We examined the effect of N-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase, on micturition reflexes induced by continuous infusion of saline or 0.1% acetic acid (a noxious stimulus) into the bladder in urethane-anesthetized female rats. Bladder and external urethral sphincter function were monitored with a continuous cystometrogram (CMG) and electromyography (EMG). RESULTS: Intrathecal injection of L-NAME (0.01 to 1 mumol.) did not significantly change the CMG or sphincter EMG during saline infusion. Infusion of acetic acid decreased the intercontraction interval (ICI), indicating a decrease in the volume threshold for inducing micturition. Subsequent intrathecal administration of L-NAME partially reversed the decreased ICI in a dose-dependent manner, but did not change the amplitude of bladder contractions: 0.01, 0.1 and 1 mumol. of L-NAME produced increases of 25%, 31% and 56% in the ICI. D-NAME, the inactive stereoisomer had no effect. This effect of L-NAME was reversed by injection of L-arginine (2 mumol. intrathecally) which, by itself, did not alter ICI during saline infusion or acetic acid infusion. CONCLUSIONS: These results indicate that: (1) spinal NO containing pathways do not play a role in the normal micturition reflex, (2) NO is involved at the spinal level in the facilitation of the micturition reflex by nociceptive bladder afferents activated by noxious chemical irritation of the bladder.
Acetates↗
Non-NMDA glutamatergic excitatory transmission in the descending limb of the spinobulbospinal micturition reflex pathway of the rat.
I.v. administration of GYKI-52466, a non-competitive AMPA/kainate glutamatergic receptor antagonist, inhibited bladder contractions elicited by electrical stimulation in the pontine micturition center (PMC) in urethane-anesthetized rats. The mean threshold dose of GYKI-52466 was 2 mg/kg i.v. (range = 1-4 mg/kg). Maximum inhibition (mean = 57.7 +/- 8.2%, range = 24-83.3% of control) occurred at a dose of 8 mg/kg. CNQX, a competitive AMPA/kainate glutamatergic receptor antagonist, did not significantly alter the evoked contractions. These results indicate that AMPA/kainate receptors are involved in bulbospinal excitatory pathway from the PMC to the parasympathetic nucleus in the lumbosacral spinal cord in the rat.
Animals↗
Effects of GYKI 52466 and CNQX, AMPA/kainate receptor antagonists, on the micturition reflex in the rat.
GYKI 52466, a non-competitive AMPA/kainate glutamate receptor antagonist, administered in graded doses (0.5-8 mg/kg, i.v.) at 10 min intervals, decreased the amplitude and duration of reflex bladder contractions (maximal inhibition = 63%), the intercontraction interval (maximal inhibition = 83%) and external urethral sphincter activity (maximal inhibition = 91%) in urethane-anesthetized (1.2 g/kg, s.c.) intact rats during continuous transurethral cystometrograms. On the other hand, in unanesthetized decerebrate rats, the drug did not alter reflex bladder activity but did produce a significant depression of sphincter activity (maximal inhibition = 59%). The depressant effects of single doses of GYKI 52466 (4 mg/kg, i.v.) on external urethral sphincter EMG activity occurred with similar time courses in both urethane-anesthetized (1.2 g/kg, s.c.) intact and unanesthetized decerebrate rats during continuous transurethral cystometrograms. In urethane-treated (0.6 g/kg, i.p.) decerebrate rats, GYKI 52466 (0.5-4 mg/kg, i.v.) depressed bladder contraction amplitude and sphincter EMG activity, similar to the effects in urethane-anesthetized (1.2 g/kg, s.c.) intact rats. CNQX (0.01-1 mg/kg, i.v.), a competitive AMPA/kainate receptor antagonist, administered to urethane-anesthetized (1.2 g/kg, s.c.) intact or unanesthetized decerebrate rats did not alter the bladder or the external urethral sphincter activity during continuous transurethral cystometrograms, possibly due to the inability of the drug to readily cross the blood-brain barrier. The present results indicate that glutamatergic excitatory transmission mediated by AMPA/kainate receptors is essential for the activation of external urethral sphincter activity during micturition in anesthetized and unanesthetized preparation. However, the depressant effect of GYKI 52466 on reflex bladder activity is only unmasked by urethane anesthesia, raising the possibility that urethane interacts with AMPA/kainate glutamate receptors in the spinobulbospinal micturition reflex pathway.
6-Cyano-7-nitroquinoxaline-2,3-dione↗
Influence of spinal cord injury on the morphology of bladder afferent and efferent neurons.
Severe micturition dysfunction can occur following spinal cord injury (SCI) due to abnormal contractions of the urethral sphincter during bladder contractions (bladder/sphincter dyssynergia). This causes urinary retention, bladder overdistension, and increases the workload of the bladder leading to hypertrophy of the bladder muscle. Bladder hypertrophy induced by urethral outlet ligation in rats is accompanied by enlargement of both the afferent and efferent neurons innervating the bladder. The primary aim of this study was to test whether SCI-induced bladder hypertrophy produces a similar enlargement of bladder afferent neurons in the dorsal root ganglia (DRG) or efferent neurons in the major pelvic ganglia (MPG). Following SCI in female Wistar rats, there was a four-fold increase in bladder weight. The mean cross-sectional area of bladder DRG cell profiles increased approx. 50% after SCI; however, the mean area of MPG cell profiles did not change significantly. Urinary diversion (disconnecting the ureters from the bladder) prevented both the bladder hypertrophy and the DRG cell hypertrophy after SCI, suggesting that bladder hypertrophy drives DRG cell enlargement. On the other hand, since the size of MPG cells did not change significantly after SCI, bladder hypertrophy does not mandate MPG cell enlargement. However, preliminary results indicate that the mean cross-sectional area of MPG cells did increase (2-3 times) in SCI rats when the neural input to the MPG was eliminated by transecting the pelvic and hypogastric nerves; this suggests that the lack of change in size of MPG cells after SCI may be due to an inhibitory influence from the spinal cord.
Afferent Pathways↗
Transneuronal labeling of neurons in the adult rat brainstem and spinal cord after injection of pseudorabies virus into the urethra.
Transneuronal tracing techniques were used to identify sites in the central nervous system involved in the neural control of urethral function. The distribution of virus-infected neurons was examined in the spinal cord and brainstem at various intervals (56-96 hours) following pseudorabies virus (PRV) injection into the urethra. In the lumbosacral (L6-S1) spinal cord at 56 hours, neurons containing PRV immunoreactivity (PRV-IR) were located in the region of the sacral parasympathetic nucleus (SPN), around the central canal, and in the dorsal commissure. Some animals also exhibited PRV-IR in cells in the L6 dorsolateral motor nucleus. At longer survival times (72-96 hours), PRV-IR cells were observed in the superficial and deeper laminae of the dorsal horn, and increased numbers of PRV-IR cells were consistently detected in the region of the SPN, around the central canal, and in the dorsal commissure. PRV-IR fiber-like staining also occurred along the lateral edge of the dorsal horn extending from Lissauer's tract to the region of the SPN. In rostral lumbar segments (L1-L2), PRV-IR cells were located in the region of the dorsal commissure and the intermediolateral cell nucleus (IML), around the central canal, and in the dorsal horn. After 72-84 hours, PRV-IR cells were also noted at more rostral levels of the neuraxis including the medulla, pons, midbrain, and diencephalon. At 72 hours, PRV-IR cells were consistently observed in Barrington's nucleus (pontine micturition center), nucleus raphe magnus (RMg), parapyramidal reticular formation, and the A5 and A7 regions. At 78-84 hours, additional regions exhibited PRV-IR cells, including the periaqueductal gray, locus coeruleus, the dorsal and ventral subcoeruleus alpha, and the red nucleus. A few cells were also located in the lateral hypothalamic area. This distribution of PRV-labeled cells in the spinal cord and brainstem is similar in many respects to the distribution of cells labeled in previous studies by PRV injection into the urinary bladder. This overlap of urethra and bladder neurons is consistent with the results of physiological experiments indicating a close coordination between the central nervous control of bladder and urethral activity.
Animals↗