Greater disorderliness of ACTH and cortisol release accompanies pituitary-dependent Cushing''s disease

BACKGROUND: We examined the mechanism of urinary bladder motility return after bladder areflexia induced by interruption of the sacral parasympathetic outflow to the urinary bladder following damage to the sacral cord or pelvic nerves in the rat. METHODS: The L6 and S1 nerve bundles were resected near the vertebrae, and bilateral pelvic nerve resections (PNR) performed. Spinal cord injury (SCI) was performed by means of a legion generator at the T12 vertebra. Thirty days after PNR and SCI, cystometrograms were recorded under anesthesia. RESULTS: In all rats subjected to PNR or SCI, overflow incontinence continued, yet some rats subjected to SCI recovered within 2 weeks after the operation. Cystometrograms showed that repetitive bladder contractions appeared in rats subjected to SCI irrespective of hypogastric nerve (HGN) innervation, while bladder contractions did not appear in rats subjected to PNR. Electrical stimulation of the HGN induced higher bladder pressure elevation in rats who underwent PNR than in rats subjected to SCI. CONCLUSIONS: These results suggest that the generation of repetitive bladder contractions induced by bladder distention after bladder areflexia requires the presence of intact pelvic nerves that transmit sacral cord-originating excitatory information to the bladder. However, the HGN system and functioning pelvic nerve ganglia are not involved in this process. Also, the connection from the preganglionic HGN to the postganglionic parasympathetic nerves in the pelvic plexus did not form after PNR.     

Nervous regulation of the tone of the retractor penis muscle in the goat

The nervous control of the retractor penis muscle (rp) was investigated in the anaesthetized goat. Also, isolated field stimulated strips of the muscle were studied. The noradrenaline (NA) and acetylcholine (ACh) content of the rp was determined, and histochemistry for adrenergic and acetylcholinesterase (AChE) positive nerves was performed. The muscle exhibited spontaneous activity that persisted after section of all nerves. There was, however, also a tendency of the activity to follow the general vasomotor tone, which disappeared after section of the sympathetic chains. The excitatory adrenergic nerves which innervate the muscle come from the sympathetic chains and run along the pudendal, the hypogastric and the pelvic nerves. The rp has a dense network of adrenergic fibres and is very sensitive to excitatory adrenergic stimulation. It has a fairly large NA content, which is higher in old goats (5.95 +/- 0.42 micrograms g-1) than in young goats (2.87 +/- 0.78 micrograms g-1). Inhibitory non-adrenergic non-cholinergic (NANC) innervation reaches it via the pelvic and the hypogastric nerves. The maximum inhibitory response is reached at low frequencies (2-4 Hz). Cholinergic prejunctional inhibition of the excitatory response to sympathetic chain stimulation was effected by simultaneous stimulation of the hypogastric nerves. In vitro experiments confirmed the presence of endogenous cholinergic muscarinic suppression of the excitatory adrenergic neurotransmission. Significant amounts of ACh (0.81 +/- 0.18 micrograms g-1) are present in the muscle, and it contains strongly AChE positive nerve fibres and nerve cell bodies. It is concluded that the goat rp is innervated by sympathetic adrenergic excitatory nerves and parasympathetic NANC inhibitory nerves. It further has a direct sympathetic inhibitory NANC innervation, and an indirect inhibitory cholinergic innervation which at least in part is sympathetic.     

Re-intervention in the anal region

In 29 rats, responses evoked by pelvic and hypogastric nerve stimulation were recorded from postganglionic nerves to bladder and penis (clitoris). Responses to pelvic nerve stimulation had nonsynapsing and synapsing components. The nonsynapsing component was relatively large in main nerve to penis and small in lateral nerve to penis and nerves to bladder. Pelvic nerve fiber synapsing on pelvic ganglion neurons to bladder had a large subliminal fringe, while fibers synapsing on neurons supplying penis (clitoris) had a small subliminal fringe. Recruitment was greater in nerves to bladder and lateral nerve to penis (clitoris) compared to main nerve to penis (clitoris), indicating more synapsing fibers in the former nerves. Almost all hypogastric fibers to bladder were direct. A small subliminal fringe was demonstrated for hypogastric fibers synapsing on neurons supplying penis. No subliminal fringe was evident for the bladder. Pelvic and hypogastric nerve interaction on pelvic ganglion neurons could not be demonstrated with either single shock or tetanic trains of conditioning stimuli. With antidromic stimulation, conduction velocities of afferent fibers in pelvic nerve ranged from 0.15 m per sec to 2.9 m per sec. In hypogastric nerve they ranged from 0.35 m per sec to 2.8 m per sec.     

Effects of ketamine on somatosympathetic reflex discharges in cats

Effects of ketamine on somatosympathetic reflex discharges induced from sympathetic trunk with electrical stimulation of superficial peroneal nerve were investigated in 51 cats under anesthesia with urethane and alpha chloralose. These reflex discharges through spinal cord and medulla oblongata consist of two components, A and C reflexes, which are derived from somatic myelinated and unmyelinated afferent fiber respectively. Amplitudes of both A and C reflex potentials were depressed significantly after intravenous injection of ketamine 10 mg.kg-1. The maximum depression was observed 5 min after administration. In decerebrated cats with surgical transection at the midbrain, both A and C reflexes were also depressed after administration of the same dosages, and the maximum level of the depression was more profound than that in brain intact cats. After intrathecal injection of ketamine 1 mg.kg-1 to the lumbar spinal region, a slight depression of C reflex was found, but, dosages of 10 mg.kg-1 significantly depressed both A and C reflexes to the similar levels as those in iv injection to brain intact cats. The maximum depression was observed 30 min after administration. The depressive effects on both reflexes of intravenous ketamine 10 mg.kg-1 were not antagonized by naloxone 0.06 mg.kg-1 in brain intact cats. These results suggest that the suppressive effects of ketamine on somatosympathetic reflexes are caused by direct inhibition of medulla oblongata and spinal cord, whereas supra-midbrain regions may be activated by ketamine, and the effect of ketamine is predominant on medulla oblongata in this situation rather than on the spinal cord.     

Sacral glutamatergic transmission in the descending limb of the micturition reflex in the cat

This study was undertaken to clarify the location of glutamatergic synaptic transmission in the descending pathway of the micturition reflex in decerebrate cats. Contractions of the urinary bladder evoked by stimulating the pontine micturition center were completely inhibited by the broad-spectrum excitatory amino acid antagonist, kynurenic acid (KYN) and the selective N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801, that were applied intrathecally to the sacral cord, while such contractions were not attenuated by the non-NMDA receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). An iontophoretic application of KYN remarkably inhibited discharges of the sacral parasympathetic preganglionic neurons innervating the urinary bladder (bladder motoneurons) elicited by pontine stimulation. Our results suggest that glutamatergic synaptic transmission is located at the level of the sacral cord in the descending limb of the micturition reflex and is mediated via NMDA receptor on the bladder motoneurons.     

Baroreceptor effects on renal and adrenal nerve activity

Spontaneous efferent discharges were recorded from nerve filaments dissected from adrenal and renal nerve bundles in the rabbit. Raising of the systemic blood pressure or stimulation of the depressor nerve caused a decrease in discharge rate in these nerve filaments. Portal vein occlusion or elevation of mesenteric venous pressure caused a depression of activity in these nerves. It is suggested that adrenal and renal sympathetic nerve cells receive inputs from baroreceptors in the systemic arterial system and from mechanoreceptors in the portal and mesenteric veins that cause reflex inhibition of activity in these nerve cells.     

The inhibitory effect of nociceptin on the micturition reflex in anaesthetized rats

1. We have investigated the effect of nociceptin on the micturition reflex evoked by distension or topical application of capsaicin on the urinary bladder of urethane-anaesthetized rats. 2. Nociceptin produced a dose-dependent (3-100 nmol kg(-1) i.v.) transient suppression of the distension-evoked micturition reflex: its effect was not modified by guanethidine (68 micromol kg(-1) s.c.) nor by bilateral cervical vagotomy, alone or in combination, and by naloxone (1.2 micromol kg(-1) i.v.). 3. Nociceptin (100 nmol/kg i.v.) slightly (about 30%) inhibited the contractions of the rat bladder produced by pre- or postganglionic electrical stimulation of the pelvic nerve. 4. Nociceptin almost totally abolished the reflex component of the response to topical capsaicin (1 microg in 50 microl). 5. In the rat isolated bladder, submaximal contractions produced by electrical field stimulation were slightly reduced (25+/-4% inhibition) by 1 microM nociceptin. Nociceptin did not affect the contraction of the rat bladder induced by acetylcholine (10 microM) or ATP (1 mM). 6. These findings indicate that nociceptin exerts a naloxone-resistant suppression of the volume-evoked micturition reflex which involves inhibition of transmitter release from postganglionic bladder nerves. An inhibitory effect on bladder afferent nerves is also suggested.     

Three types of reticular neurons involved in the spino-bulbo-spinal reflex of cats

Reticular neuron activity was recorded in 28 chloralosed cats in order to analyze the reflex arc of the spino-bulbo-spinal (SBS) reflex. Three types of reticular neurons, types I (input), II(output) and III (relay), were identified by unit discharges in response to stimulation of the sural nerve. (1) Type I (input) neurons received spinal ascending volleys monosynaptically and responded to stimulation of the sural nerve with spikes of low amplitude and short latency. Unit spikes, however, were not produced by stimulation of the superficial radial nerve and the sensorimotor cortex. These input neurons were located in the dorsocaudal part of the medial bulbar reticular formation. (2) Type II (output) neurons were part of the reticulospinal tract, which sends axons to the spinal cord, since these neurons exhibited antidromic spikes following stimulation of the ventrolateral funiculus of the spinal cord. Unit spikes were evoked by stimulation either to the sural or superficial radial nerves. These neurons were located in the ventrocaudal part of the medial bulbar reticular formation. (3) Type III neurons included relay neurons. Unit spikes were evoked by stimulation of the sural nerve, superficial radial nerve and sensorimotor cortex. However, unit discharges were not obtained by antidromic stimulation to the reticulospinal tract. These neurons were distributed widely in the brain stem, both in the bulb and pons. (4) Latency difference of unit discharges between input and output neurons was 3.5--5 msec, indicating the presence of interneurons (relays) between input and output neurons. Spikes of output neurons with 3.8--4.2 msec latency were observed following stimulation of the region where input neuron activity was found. We may conclude that three kinds of reticular neurons, input, relay and output, were involved in pathways of the SBS reflex.     

Mechanosensitive afferent units in the hypogastric nerve of the cat

1. Recordings have been made from ninety single afferent units in the hypogastric and lumbar splanchnic nerves of the cat. 2. The majority of units examined had properties similar to those previously described in the splanchnic nerve: they were slowly adapting mechanoreceptors with one to six punctate mechanosensitive sites distributed mainly along blood vessels as they approached the viscera in peritoneal ligaments; they had a wide range of mechanical thresholds and conduction velocities in the range 0.5-24 m s-1. 3. Receptive fields were found over the bladder base or its peritoneal ligaments or both, on the uterus or broad ligament or both, on the colon or mesocolon or both, and in association with the ureter, vas deferens, prostate or pelvic fat pads. 4. Discharges from afferent units associated with the bladder were investigated during spontaneous (or reflex) bladder contractions, passive distensions, and tetanic contractions induced by electrical stimulation of the sacral spinal cord. The mean spike rates of the adapted (tonic) discharges, observed during distensions and induced tetani, differed over part of the range of intravesical pressures examined. Their behaviour is discussed in relation to the concept of 'in series' tension receptors within the bladder wall.     

Neural mechanism of pupillary dilation elicited by electro-acupuncture stimulation in anesthetized rats

The neural mechanisms to reflex dilation elicited by electro-acupuncture stimulation were investigated in anesthetized rats. Two needles, with 160 microns diameter and about 5 mm apart, were inserted into the skin and underlying muscle of a hindpaw. Repetitive 20 Hz, 0.5 ms electrical pulses at various intensities were used for stimulation for 30s. The pupil size was magnified about 44 times via a microscope and was continuously recorded on a videotape. Electro-acupuncture stimulation at more than 0.5 up to 6 mA induced stimulus intensity-dependent pupil dilation. These responses were abolished by the severance of the sciatic and saphenous nerve of the stimulated hindlimb. Compound action potentials were recorded from the distal cut end of the tibial of a saphenous nerve following electro-acupuncture stimulation of the hindpaw. The mean threshold of the compound action potentials of the myelinated fibers in saphenous nerves was 0.18 mA, while that of unmyelinated fibers was 3.0 mA. The mean threshold of the compound action potentials of the myelinated fibers in the tibial nerve was 0.20 mA of unmyelinated fibers was 3.3 mA. Severance of bilateral trunks did not affect the response, while severance of the third cranial nerves abolished the responses. In conclusion, electro-acupuncture stimulation applied to the hindpaws of the anesthetized rats induced excitation of myelinated or of both myelinated and unmyelinated afferent fibers of the tibial and saphenous nerve, and involved a reflex response of pupil dilation through the third cranial parasympathetic efferent nerve.     

Neuroexcitatory effects of digoxin in the cat

The effect of intravenous injections of digoxin (20 mug/kg every 15 minutes) on spontaneously occurring activity in autonomic efferent nerves, motor nerves, afferent nerves, electrocardiogram and on arterial blood pressure was evaluated in chloralose-anesthetized cats. Administration of digoxin enhanced neural activity in pre- and postganglionic cardiac synpathetic nerves and this enhancement occurred near the time the disturbances in ventricular rhym were noted. Neural activity continued to increase during ventricular tachycardia and maximum enhancement was observed just proir to ventricular fibrillation. Similar results were observed when digoxin was administered to animals in which neural activity was recorded from preganglionic splanchnic and superior cervical nerves. Digoxin administration also increased discharge frequency from vagus (efferent fibers), phrenic and carotid sinus nerves. Denervation of cardiovascular reflexogenic areas prevented the increased discharge in vagus nerves, reduced it in phrenic nerves, but did not affect nerve discharge in sympathetic nerves. These results suggest that digoxin-induced hyperactivity in synpathetic nerves was related to a central nervous system effect of the drug, whereas the mechanism for the digoxin-induced hyperactivity in vagus nerves involved a peripheral reflex effect of the drug. Both sites were involved in the digoxin-induced hyperactivity in phrenic nerves. Enhancement of cardiac sympathetic nerve activity appeared to be responsible for the ventricular arrhythmias provoked by digoxin as 1) a temporal relationship was observed between augmented nerve activity and arrhythmia development, 2) a centrally acting sympathetic nervous system depressant drug, clonidine, converted the ventricular arrhythmia to normal rhythm, and 3) removal of sympathetic influence to the heart by spinal cord transection decreased the sensitivity of the heart to the arrhythmogenic effect of digoxin. These results suggest that digoxin partially responsible for its cardiotoxic effects.     

Differential c-fos expression in the nucleus of the solitary tract and spinal cord following noxious gastric distention in the rat

c-Fos has been used as a marker for activity in the spinal cord following noxious somatic or visceral stimulation. Although the viscera receive dual afferent innervation, distention of hollow organs (i.e. esophagus, stomach, descending colon and rectum) induces significantly more c-Fos in second order neurons in the nucleus of the solitary tract and lumbosacral spinal cord, which receive parasympathetic afferent input (vagus, pelvic nerves), than the thoracolumbar spinal cord, which receives sympathetic afferent input (splanchnic nerves). The purpose of this study was to determine the contribution of sympathetic and parasympathetic afferent input to c-Fos expression in the nucleus of the solitary tract and spinal cord, and the influence of supraspinal pathways on Fos induction in the thoracolumbar spinal cord. Noxious gastric distention to 80 mmHg (gastric distension/80) was produced by repetitive inflation of a chronically implanted gastric balloon. Gastric distension/80 induced c-Fos throughout the nucleus of the solitary tract, with the densest labeling observed within 300 microns of the rostral pole of the area postrema. This area was analysed quantitatively following several manipulations. Gastric distension/80 induced a mean of 724 c-Fos-immunoreactive nuclei per section. Following subdiaphragmatic vagotomy plus distention (vagotomy/80), the induction of c-Fos-immunoreactive nuclei was reduced to 293 per section, while spinal transection at T2 plus distention (spinal transection/80) induced a mean of 581 nuclei per nucleus of the solitary tract section. Gastric distension/80 and vagotomy/80 induced minimal c-Fos in the T8-T10 spinal cord (50 nuclei/section), but spinal transection/80 induced 200 nuclei per section. Repetitive bolus injections of norepinephrine produced transient pressor responses mimicking the pressor response produced by gastric distension/80. This manipulation induced minimal c-Fos in the nucleus of the solitary tract and none in the spinal cord. It is concluded that noxious visceral input via parasympathetic vagal afferents, and to a lesser extent sympathetic afferents and the spinosolitary tract, contribute to gastric distention-induced c-Fos in the nucleus of the solitary tract. The induction of c-Fos in the nucleus of the solitary tract is significantly greater than in the viscerotopic segments of the spinal cord, which is partially under tonic descending inhibition, but is not subject to modulation by vagal gastric afferents. Distention pressures produced by noxious gastric distention are much greater than those produced during feeding, suggesting that c-Fos induction in the nucleus of the solitary tract to noxious distention is not associated with physiological mechanisms of feeding and satiety. The large vagal nerve-mediated induction of c-Fos in the nucleus of the solitary tract following gastric distension suggests that parasympathetic afferents contribute to the processing of noxious visceral stimuli, perhaps by contributing to the affective-emotional component of visceral pain.     

Reflex control of cardiac sympathetic nerve activity in anesthetized rats

Reflex control of sympathetic outflow to the heart was evaluated by recording the efferent discharges of the interior cardiac sympathetic nerves in anesthetized rats. The reflex responses of inferior cardiac sympathetic nerve activity (ICNA) to arterial baroreceptor loading by phenylephrine and to arterial/atrial baroreceptor unloading by hemorrhagic hypotension were compared with those of renal sympathetic nerve activity (RNA) and adrenal sympathetic nerve activity (ANA). The reflex decrease in ICNA to the phenylephrine-induced graded increase in arterial blood pressure was smaller than that of RNA or ANA. Thus ICNA is less sensitive to arterial baroreceptor stimulation. Hemorrhage produced a volume-dependent decrease in ICNA. The response was significantly smaller than that in RNA and was directionally opposite to that in ANA. Cervical vagotomy but not sinoaortic denervation abolished the hemorrhage-induced ICNA response, suggesting an important role of vagal pathways. These findings demonstrate that the reflex responses of sympathetic outflow to the heart were quantitively and qualitatively different from those to the kidney and the adrenal gland, indicating the regional control of sympathetic nerve activity in the regulation of cardiovascular functions.     

The central neural mechanism of the gastric motility in the dog's medulla oblongata on the vagal inhibitory and excitatory reflexes (author's transl)

The influences of the vagal inhibitory and excitatory reflexes on the gastric motor centers in the dog's medulla oblongata were investigated. Dogs were anaesthetized with Nembutal, and supplemented Gallamine at need. The brain stem was transected on the level of inferior colliculi of midbrain, the spinal cord transected on the level of between C1 and C2. Bilateral splanchnic nerves were also severed. Electrical activities from the inhibitory and excitatory areas in medulla oblongata were recorded by using a concentric circle electrode which was inserted into medulla oblongata from the dorsal surface of it. Following results were obtaind. 1) Electrical activities of the gastric inhibitory areas were classifed into three types (see Table 1). Type I: The augmentation of electrical activities of the gastric inhibitory areas during theinhibitory reflex were associated with the diminution of them during the exictatory reflex. Type II: Although electrical activities of the gastric inhibitory areas were augmented during the inhibitory reflex, any changes of them were not obtained during the excitatory reflex. Type III: Any changes of electrical activities of the gastric inhibitory areas were not obtained during both inhibitory and excitatory reflexes. 2) Electrical activities of the gastric excitatory areas were classified into two types (see Table 2). Type I: The diminution of electrical activites of the gastric excitatory areas during the inhibitory reflex were associated with the augmentation of them during the excitatory reflex. Type II: Although any changes of electrical activities of the gastric excitatory areas were not observed during the inhibitory reflex, they were augmented during the excitatory reflex.     

Genitosensory nerve modulation of paced mating behavior: Evidence for pelvic, but not hypogastric, nerve influence.

The pelvic nerve is known to play a role in the behavioral and neurochemical responses exhibited during paced mating behavior. The present study extended the analysis of the contribution of the genitosensory nerves to the display of paced mating behavior to include bilateral hypogastric nerve transection, bilateral pelvic nerve transection, or transection of both the hypogastric and pelvic nerves. Rats with pelvic nerve transection were less likely to exit the male compartment, took longer to exit the male compartment following intromissions, and returned to the male more quickly following intromissions compared to rats with an intact pelvic nerve. In contrast, hypogastric nerve transection alone did not affect paced mating and had no modulating effect on the paced mating behavior of rats with pelvic nerve transection. Our results support the view that key aspects of paced mating behavior are modulated by signals transmitted via the pelvic nerve, without any discernable contribution from the hypogastric nerve. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Canal-specific excitation and inhibition of frog second-order vestibular neurons

Second-order vestibular neurons (secondary VNs) were identified in the in vitro frog brain by their monosynaptic excitation following electrical stimulation of the ipsilateral VIIIth nerve. Ipsilateral disynaptic inhibitory postsynaptic potentials were revealed by bath application of the glycine antagonist strychnine or of the gamma-aminobutyric acid-A (GABA(A)) antagonist bicuculline. Ipsilateral disynaptic excitatory postsynaptic potentials (EPSPs) were analyzed as well. The functional organization of convergent monosynaptic and disynaptic excitatory and inhibitory inputs onto secondary VNs was studied by separate electrical stimulation of individual semicircular canal nerves on the ipsilateral side. Most secondary VNs (88%) received a monosynaptic EPSP exclusively from one of the three semicircular canal nerves; fewer secondary VNs (10%) were monosynaptically excited from two semicircular canal nerves; and even fewer secondary VNs (2%) were monosynaptically excited from each of the three semicircular canal nerves. Disynaptic EPSPs were present in the majority of secondary VNs (68%) and originated from the same (homonymous) semicircular canal nerve that activated a monosynaptic EPSP in a given neuron (22%), from one or both of the other two (heteronymous) canal nerves (18%), or from all three canal nerves (28%). Homonymous activation of disynaptic EPSPs prevailed (74%) among those secondary VNs that exhibited disynaptic EPSPs. Disynaptic inhibitory postsynaptic potentials (IPSPs) were mediated in 90% of the tested secondary VNs by glycine, in 76% by GABA, and in 62% by GABA as well as by glycine. These IPSPs were activated almost exclusively from the same semicircular canal nerve that evoked the monosynaptic EPSP in a given secondary VN. Our results demonstrate a canal-specific, modular organization of vestibular nerve afferent fiber inputs onto secondary VNs that consists of a monosynaptic excitation from one semicircular canal nerve followed by disynaptic excitatory and inhibitory inputs originating from the homonymous canal nerve. Excitatory and inhibitory second-order (secondary) vestibular interneurons are envisaged to form side loops that mediate spatially similar but dynamically different signals to secondary vestibular projection neurons. These feedforward side loops are suited to adjust the dynamic response properties of secondary vestibular projection neurons by facilitating or disfacilitating phasic and tonic input components.     

Charge transfer of 0.5-, 1.5-, and 5-keV protons with atomic oxygen: Absolute differential and integral cross sections

We investigated the electrocortical (E.Co.G) correlates of visceral (topical capsaicin application or overdistension of the urinary bladder) and somatic (perineal pinching) painful stimulation in urethane-anesthetized rats and their modulation by intrathecal application of selective tachykinins receptors (NK 1 and NK 2) antagonists. Vesical overdistension or topical capsaicin on the bladder serosal surface produced an immediate and lasting E.Co.G. desynchronization resembling a cortical arousal. A second application of capsaicin was ineffective. Bladder contraction induced by topical acetylcholine did not alter E.Co.G. A desynchronized E.Co.G. was also induced by pinching of the perineal area of the rat. Intrathecal administration of lidocaine at lumbosacral level abolished the E.Co.G. desynchronization induced by both visceral and somatic noxious stimulation. On the other hand capsaicin-induced or over-distension (but not pinching-induced) E.Co.G. desynchronization disappeared in animals systemically pretreated with capsaicin or after intrathecal administration of NK 1 tachykinin receptor antagonists such as the peptide GR 82334 or the nonpeptide RP 67580, whereas the inactive enantiomer RP 68651 or the nonpeptide NK 2 antagonists SR 48968 were ineffective. In conclusion, the experimental model described herein, allowing a quantitative analysis of the E.Co.G. correlates of visceral and somatic noxious stimulation in urethane-anesthetized rats, provides evidence for a specific neural pathway carrying bladder-arising visceral (both mechanical and chemical) nociception that uses pelvic capsaicin-sensitive afferents projecting to NK 1 (but not NK 2) bearing spinal neurons and that ultimately leads to activation of cortical areas.     

An observation on the possible existance of some information transmission between sensory nerve endings of rat

Dorsal cutaneous branches of the spinal nerves of T5-L1 segments on one side in anaesthesised rats were exposed and cut centrally. One peripheral end of the cut nerves was selected for antidromical stimulation, while an adjacent one for recording, both by Ag-AgCl electrodes. When a train of 50 Hz, 0.2 ms width square waves of 2 s was delivered to the nerve preparation for stimulation, the discharge of the adjacent nerve showed a remarkable increase and then subsided to the original level for about 25 s. Such experiments (n = 414) showed that the induced discharge frequency reached its maximum 2 s after the stimulation and maintained for another 2 s before subsiding to original level in about a period of 25 s. Using the discharge frequency at a certain time segment as an index, the degree of induced discharges of the recorded nerves were linearly related to their spontaneous discharges before stimulation and the sequences of stimulation to some extent. Single square stimulation was unable to induce one-to-one correspondent discharge in the recording nerve. Control experiments were done to rule out the induced discharges being due to the spreading of stimulating current. To summarize the results of all the above experiments, it appeared that some information transmission between sensory nerve endings may be present through some chemical events.     

(6-4) photolyase: light-dependent repair of DNA damage

Eight of 32 patients (25%) with chronic inflammatory demyelinating polyneuropathy (CIDP) had micturitional disturbance, which consisted of voiding difficulty (n = 4), urgency (n = 4), or urgency incontinence (n = 1). Urodynamic studies on four symptomatic patients showed disturbed bladder sensation in two, bladder areflexia in one, and neurogenic changes of the external sphincter in one, indicative of peripheral parasympathetic and somatic nerve dysfunctions. Cystometry also showed detrusor overactivity in two patients but no evidence of CNS involvement, evidence that bladder overactivity occurs by probable pelvic nerve irritation.     

Mechanisms of efferent neuronal control of the reflex nictitating membrane response in rabbit (Oryctolagus cuniculus).

Analyzed efferent mechanisms controlling the nictitating membrane (NM) reflex response to air puff in the albino rabbit, using stimulation, lesions, and recording techniques with 52 New Zealand male Ss in 6 experiments. In brief, stimulation of the 6th nerve (abducens) yielded short-latency NM extension. Stimulation of the 4th and 7th nerves and the superior cervical ganglion had essentially no effect on the NM. Stimulation of the 3rd nerve caused short-latency retraction of the NM. Lesions and recording data were consistent with this result--the sole efferent neuronal control of NM extension was the 6th cranial nerve and of NM retraction was the 3rd cranial nerve. It is concluded that the NM extension response appears to be mediated by mechanical actions via retraction of the eyeball by the retractor bulbi muscle, and NM retraction appears to result from direct activation of muscle fibers in the NM by the 3rd nerve. The superior cervical ganglion appears to play no role in reflex NM retraction in the rabbit, in contrast to its action in the cat. (18 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)