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T Neya

Publications and source records attributed to T Neya.

At least 37 records · Page 2Linked to original sources

Enteric opioid neurons modulate the basal tone of the isolated puppy ileum.

We studied the role of enteric opioid neurons in the spontaneous motility of the longitudinal muscle in the isolated puppy ileum. Regular fluctuations in tone that rose above and returned to the basal level occurred at an interval of 4.7 +/- 0.3 min. Naloxone (10(-8) and 10(-7) M) reduced the spontaneous tonic contraction by 42.6 +/- 11.6% (p less than 0.02) and 77.0 +/- 3.6% (p less than 0.001), respectively. Tetrodotoxin (3.1 X 10(-7) M) and atropine (10(-7) M) terminated the fluctuations. Met- and Leu-enkephalins (10(-9)-10(-8) M) caused tonic contraction which was abolished by tetrodotoxin and atropine. The contractile response produced by transmural electrical stimulation was reduced by naloxone (10(-7) M). This response was also abolished by atropine and tetrodotoxin. These results suggest that enteric opioid neurons are spontaneously active and might operate, at least in part, to raise the basal tone of the longitudinal muscle in the puppy ileum through a cholinergic excitatory mechanism.

Animals↗

Functional role of lumbar sympathetic nerves and supraspinal mechanism in the defecation reflex of the cat.

The role of the lumbar sympathetic nerves and supraspinal mechanism in the defecation reflex was investigated in 30 adult cats and 6 kittens. One or two propulsive contractions, whose mean pressure evoked was more than about 90 cmH2O (adult cats) and 50 cmH2O (kittens), were induced in the rectum of all animals by rectal distension. These propulsive contractions could be generated at the descending and the transverse colons. The removal of the supraspinal influence by spinal transection at T13 or removal of pelvic afferents to the supraspinal center by spinal transection at L abolished the propulsive contractions. Successive lumbar sympathectomy restored the contractions. Lumbar sympathectomy and the successive removal of the supraspinal influence did not affect the propulsive contractions. In both cases, the final exclusion of the sacral segments by pithing of the spinal cord abolished the propulsive contractions. These results suggest that the sacral excitatory reflex mediated via pelvic nerves and the lumbar inhibitory reflex mediated via lumbar sympathetic nerves can function during rectal distension in spinal cats and that the lumbar inhibitory reflex is suppressed by the supraspinal sympathetic inhibitory reflex activated by pelvic afferents in intact cats, as in guinea pigs, resulting in propulsive contractions.

Afferent Pathways↗

Pelvic afferent reflex control of rectal motility and lumbar colonic efferent discharge mediated by the pontine sympatho-inhibitory region in guinea pigs.

Rectal motility and the efferent discharge of lumbar colonic nerves (LCED) have previously been shown to be affected by reflex activity activated by rectal stimulation. The sensory limb of this reflex is represented by afferent fibers in pelvic nerves. The present study revealed that this reflex is modulated by supraspinal sympatho-inhibitory regions. Pelvic afferent stimulation led to rectal contraction through the withdrawal of a tonic inhibitory influence of lumbar colonic nerves. The supraspinal region responsible for this antagonism of the rectal-inhibitory colonic nerve activity was localized to the pons. Neither the intravenous administration of atropine nor that of guanethidine (and Eisai compound 865-123, another adrenergic neuron blocking agent) effected the ability of pelvic afferent stimulation to inhibit tonic discharge of lumbar colonic efferent nerves; nevertheless, both agents eliminated the mechanical response of the rectum to stimulation of pelvic afferents. These observations suggest that lumbar sympathetic nerves may tonically inhibit the release of acetylcholine from excitatory neurons in the rectal myenteric plexus. We conclude that descending fibers from the pons are activated as a result of pelvic afferent nerve stimulation. These descending pontine fibers in turn inhibit the firing of sympathetic lumbar colonic nerves. Removal of this tonic restraint leads to rectal contraction.

Afferent Pathways↗

[Effects of cisapride on the motility of the digestive tract in dogs and guinea pigs].

Effects of cisapride on the motility of the digestive tract in vivo in dogs and the guinea-pig intestine in vitro were studied. Cisapride (0.05-2.0 mg/kg, i.v.) produced an increase in amplitude of spontaneous contractions and basal tone in the stomach, duodenum, jejunum and proximal and distal colon in dogs. In some animals, however, it induced an inhibition with decrease in amplitude and tone. It also induced an increase in amplitude of contractions in the gallbladder and the sphincter of Oddi in dogs. The tone of the gallbladder was elevated by the same dose of cisapride, but the tone of the sphincter of Oddi was decreased. The drug produced a reverse response in some animals. These excitatory responses to cisapride were abolished by atropine (0.2 mg/kg, i.v.). Motility of the guinea-pig isolated ileum and colon was enhanced with an increase in their amplitude of contractions and basal tone at low concentrations of cisapride (10(-9)-10(-6)M) but it was inhibited at higher concentrations (10(-5)-10(-4)M). Atropine abolished the excitatory response of the ileum to cisapride in all cases. It abolished the excitation of the colon in some preparations but reduced only in some degree in the other. The inhibitory effect of cisapride on isolated preparations was unaffected by tetrodotoxin. From these results, it is concluded that cisapride enhances motility of the gastrointestinal tract and biliary tract by acting on myenteric cholinergic neurons and inhibits it by acting on the smooth muscle itself.

Animals↗

Effects of caerulein on the gastric motility of rats.

The effects of caerulein on gastric motility in urethane-anesthetized rats were studied. Caerulein administered into the lateral cerebral ventricle (i.c.v.) and jugular vein (i.v.) caused predominantly an inhibitory effect on gastric motility but sometimes an excitatory or a biphasic effect. The inhibitory response was reduced after vagotomy and/or splanchnicotomy, or after guanethidine. The remaining inhibitory response was abolished by tetrodotoxin, but was resistant to atropine and guanethidine. The excitatory response was abolished by atropine. Discharges of the gastric branch of the vagus nerve were decreased by i.v. injection of caerulein but increased by i.c.v. injection, whereas those of the splanchnic nerve were increased by both i.v. and i.c.v. injection. These results suggest that caerulein causes an inhibition of gastric motility by centrally stimulating vagal non-adrenergic inhibitory nerves and splanchnic adrenergic nerves and inhibiting vagal cholinergic nerves, and by peripherally stimulating non-adrenergic inhibitory neurons of the myenteric plexus. This peptide causes an excitation by stimulating cholinergic neurons of the myenteric plexus.

Animals↗

The effect of cecal volume change on gastric motility in rats.

The effect of a change in cecal volume on gastric motility was studied in 24 h fasted rats anesthetized with urethane (0.8 g/kg, i.p.). A cecal volume increase from 1 to 10 ml (in 1 ml steps) produced a decrease in the basal tone of the stomach. The maximal inhibitory response was produced with an 8 to 10-ml increase in cecal volume. The gastric inhibitory response continued as long as the increased cecal volume was maintained. It was abolished by a combination of a splanchnicotomy and vagotomy, or only a splanchnicotomy in a few cases. The inhibition of gastric motility by increasing the cecal volume also occurred after severance of dorsal roots between T8 and L4 and gastric branches of vagus nerves. It is suggested that an increase in cecal volume induces gastric relaxation mainly via the splanchnico-splanchnic pathway and partly via the vago-vagal and vago-splanchnic pathways. Therefore, retardation in transit of the gastric contents in germ free rats having an enlarged cecum may be attributed to an enhancement of the ceco-gastric inhibitory reflex. The ceco-gastric inhibitory response mediated by the splanchnic pathway was abolished by guanethidine (3-5 mg/kg, i.v.), but the response mediated by the vagal pathway was resistant to guanethidine as well as to atropine (0.2 mg/kg, i.v.). This result indicates that splanchnic postganglionic efferents are adrenergic, while vagal postganglionic efferents are non-adrenergic and non-cholinergic.

Animals↗

Atropine-sensitive, tetrodotoxin-resistant contraction induced by noradrenaline in isolated cat rectum.

Effects of noradrenaline (NA) on the isolated rectal circular muscle of the cats were studied in comparison with the effects on the internal anal sphincter (IAS). NA (10(-8)-10(-7) g/ml) caused tonic contraction in four of 15 strips of the rectum taken from 15 animals, and in all 15 strips of the IAS. Phenylephrine also induced rectal and IAS contraction. Rectal contraction induced by NA was resistant to phentolamine, yohimbine, propranolol, hexamethonium and tetrodotoxin, but blocked by atropine. IAS contraction induced by NA was resistant to propranolol, atropine, hexamethonium and tetrodotoxin, but blocked by phentolamine and yohimbine. It is suggested that an atropine-sensitive excitatory adrenergic mechanism other than the excitatory alpha-adrenergic mechanism exists in the rectal circular muscle.

Acetylcholine↗

Action of enkephalinergic neurons on the gastrointestinal motility.

The actions of the enkephalinergic neurons in the myenteric plexus on the gastrointestinal motility were studied using the opiate antagonist naloxone in the guinea pig in vitro and in vivo. Naloxone increased or decreased spontaneous contractions of the isolated small intestine. Both responses were abolished by atropine. Naloxone potentiated or inhibited the twitch response to transmural stimulation at a frequency of 0.1 Hz and the contractile response of the ileum to the mesenteric nerve stimulation. Naloxone reversed an inhibition of the twitch response occurred after repetitive transmural stimulation (10 Hz) for 5 minutes in the isolated ileal segment. The peristaltic reflex response in the isolated jejunum induced by its distention was reduced by repeated distention. This reduction was reversed by naloxone. Naloxone also potentiated the contractile response of the stomach to efferent vagal stimulation in vivo. It is concluded from the present results that enkephalinergic neurons in the myenteric plexus may regulate the gastrointestinal motility by inhibiting release of acetylcholine from myenteric cholinergic neurons, and that naloxone has both opiate antagonistic and partial agonistic effects on the gastrointestinal motility of the guinea pig.

Animals↗

Mechanism of rectal contraction mediated by sympathetic efferents from rectoanal pelvic afferents in guinea pigs.

In guinea pigs whose pelvic nerves were bilaterally sectioned, afferent stimulation of rectoanal branches of the pelvic nerve (PAS) could produce an intense contraction in the rectum similar to propulsive contractions elicited during defecation. The mechanism of this reflex was analyzed. Rectal contraction by PAS was abolished after transecting the spinal cord at T13 or sectioning the lumbar splanchnic nerves (LSN) or lumbar colonic nerves (LCN), but was unaffected by severing the intermesenteric and hypogastric nerves. Rectal contraction induced by PAS was abolished peripherally by atropine, guanethidine or yohimbine, while propranolol had no affect. Yohimbine antagonized the inhibitory effect of LSN or LCN stimulation on atropine-sensitive rectal contractions. It may, therefore, be concluded that PAS blocks the inhibition, by LCN efferents acting through alpha-adrenoreceptors, of cholinergic neurons in the myenteric plexus, thus facilitating recto-rectal propulsive contractions initiated by the defecation reflex.

Anal Canal↗

Role and localization of a region in the pons which has a descending inhibitory influence on sympathetically mediated inhibition of the recto-rectal reflex of guinea pigs.

The present study revealed the site of origin and the possible function of a supraspinal descending-inhibitory influence over the lumbar sympathetic component of the recto-rectal reflex of guinea pigs. The recto-rectal reflex contraction was not changed by suprapontine transection. It completely disappeared after subpontine transection, but returned immediately after additional section of the colonic nerves, which contain the sympathetic inhibitory outflow to the rectum, i.e., subpontine transection with the lumbar colonic nerves transected did not suppress the recto-rectal reflex. These results indicate that a descending pathway which can inhibit the lumbar sympathetic component of the reflex may originate in the pons. On stimulation at sites within the pons of animals which had been spinalized at L4 we were able to evoke an increase of rectal motility and an inhibition of the lumbar colonic efferent discharges, thus producing a response which is comparable to the reflex response produced by afferent stimulation of the rectum. The sites from which this effect could be evoked were mainly located in a band running rostrocaudally through the lateral reticular formation of the rostral part of the pons, medial to the sensory nucleus of the trigeminal nerve.

Animals↗

Effect of motilin on the sphincter of Oddi in the dog.

To investigate the action of motilin on the sphincter of Oddi, the flow rate of the perfusate (FRP) discharged into the duodenal lumen through the orifice of the common bile duct was measured by means of an electric drop counter in decerebrated dogs. Motilin in doses above 0.5 micrograms/kg i.v. reduced or stopped the FRP. The fifty percent recovery time of FRP was 20 min and full recovery time was 30 min. The reduction of FRP induced by motilin was unaffected by denervation and atropinization. These results suggest that motilin caused an increase in tone of the sphincter of Oddi by acting on the sphincter muscle.

Ampulla of Vater↗

Sympathetic activity in the recto-rectal reflex of the guinea pig.

In the guinea pig, defecation is controlled by the myenteric plexus, whose activity is modulated by the sacral spinal and supraspinal centers. The purpose of this study is to clarify the control of defecation reflex by sympathetic nerves. The propulsive contractions of the rectum produced by rectal distension (recto-rectal excitatory reflex response) were abolished after transection of the Th 13 and/or L 4 segment. This response was reproduced again after removal of the lumbar segments (L1--4), division of the lumbar dorsal roots (L1--4), the lumbar splanchnic nerves or lumbar colonic nerves (LCN). The frequency of efferent discharges of LCN was increased slightly by rectal distension and remarkably increased after Th 13 and/or L 4 transection. Thus, there occurs during the recto-rectal reflex not only mucosal intrinsic reflex and sacral excitatory reflex via the pelvic nerves but also a lumbar inhibitory reflex via the colonic nerves, whose center may be located in the upper lumbar segments. But, the activity of the inhibitory center was depressed by the supraspinal center, so that an excitatory reflex is produced more dominantly than an inhibitory one in normal animals. All these extrinsic reflexes coordinate the activity of the myenteric plexus in defecation reflex.

Action Potentials↗

The effect of intraluminal pressure upon the frequency of intestinal contraction waves.

In guinea pigs the lumen of an excised jejunal segment was perfused to study the effect of intraluminal pressure on the frequency of rhythmic contraction waves. Within the range of 0 to 40 mmH2O, increases in intraluminal pressure caused increases in the frequency of contraction waves. At pressures of 10, 15, 20, 30 and 40 mmH2O the frequency was 7.9, 9.0, 10.9, 12.5 and 13.3 per min (mean of ten preparations), respectively. An exponential relationship was proved to exist between the pressure and the frequency.

Animals↗

Activity patterns of temperature-reactive dorsal horn neurons and their reactions to peripheral receptor stimulation by Ca.

Unit responses of dorsal horns neurons (DHNs) of rats to thermal stimulation of the scrotal skin were recorded extracellularly. Fifty-five out of 74 DHNs increased their activity during scrotal skin warming, while the activity of 14 neurons was accelerated by cooling. Tonic activities of 3 neurons were inhibited by warming (inverse warm-reactive). Two neurons demonstrated a complex response and were activated during cooling and warming. Most of the warm-reactive and all of cold-reactive DHNs had step sigmoid temperature-activity-relation curves with a temperature-dependent range of 1-5 degrees C. Injections of 5-10 mg/kg CaCl2 into the lower abdominal aorta produced excitation in 30 out of 33 warm-reactive DHNs and inhibition in 3 neurons. Only 3 out of 8 cold-reactive DHNs demonstrated inhibition, while the remaining 5 were activated. All three inverse warm-reactive neurons were inhibited. DHNs which exclusively reacted to mechanical stimuli or did not respond to any peripheral stimulation were not affected by peripheral Ca administration. The results suggest that a number of cold-reactive DHNs receive inputs from warm- and cold-sensitive afferents and that there may exist such double innervation in some warm-reactive DHNs as well.

Animals↗

[Effects of domperidone on gastrointestinal and gallbladder motility and gastric emptying (author's transl)].

Effects of domperidone on gastric emptying and gastric, duodenal and gallbladder motility were investigated. Intravenous injection of domperidone 2 mg/kg produced an acceleration of gastric motility without increase in the tone while a marked increase in the amplitude of peristaltic waves with a slight decrease in frequency was observed. Domperidone also produced an acceleration of duodenal and gallbladder motility. Domperidone produced an acceleration of transit of stomach contents in some cases, while in others gastric emptying was inhibited. This difference of the effect may be due to the previous tone of the pylorus. The excitatory action of domperidone on gastrointestinal motility was suppressed to some degree after cervical vagotomy or vagus cooling and markedly inhibited by atropine. Tetrodotoxin reduced the excitatory effect of domperidone but did not abolish. Therefore, it is presumed that domperidone stimulates, at least in part, the gastrointestinal muscle itself as well as cholinergic neurons in the gastrointestinal wall or cholinergic receptors of the gastrointestinal muscle and that domperidone may also have a central nervous system stimulant action. On the other hand, domperidone appears to act directly on the gallbladder muscle.

Action Potentials↗

Effects of vagotomy on feeding and defecation in guinea pigs.

The effect of subdiaphragmatic vagotomy on food intake and defecation was studied in guinea pigs. Weights of food and feces were measured for at least three weeks after vagotomy. The weight of daily food intake and feces evacuated increased about 15 and 30% after vagotomy compared with controls whereas it did not change in sham operated animals. The weight of scybalum decreased after vagotomy although the number increased markedly. It was considered that an increase in food intake after vagotomy may result from blocking of satiety signals mediated by the vagus; moreover, that the increase in feces may depend on the enhancement of scybalum formation in the proximal colon resulting from increasing food intake and transportation of the larger amount of the contents after vagotomy.

Animals↗