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Biomedical subjects

M Takaki

Publications and source records attributed to M Takaki.

At least 109 records · Page 6Linked to original sources
PubMed1987

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↗
PubMed1987

Opiate-like inhibitory effect of trimebutine on the twitch response of the isolated guinea pig ileum.

Trimebutine at low concentrations (6 X 10(-9)-1.4 X 10(-8) M) slightly enhanced the twitch response of isolated guinea pig ileum induced by transmural stimulation. At high concentrations (2 X 10(-8)-2 X 10(-7) M), however, it inhibited the twitch response in a dose dependent manner. This inhibitory effect of trimebutine was reversed by naloxone (8.1 X 10(-9) M). These results suggest that trimebutine has an opiate-like action on the myenteric plexus.

Animals↗
PubMed1985

The enteric neural receptor for 5-hydroxytryptamine.

An enteric neural receptor for serotonin (5-HT) has been characterized. This receptor was assayed, using 3H-5-HT as a radioligand, by rapid filtration of isolated enteric membranes and by radioautography. In addition, intracellular recordings were made from ganglion cells of the myenteric plexus. High affinity, saturable, reversible, and specific binding of 3H-5-HT was demonstrated both to membranes of the dissected longitudinal muscle with adherent myenteric plexus and the mucosa-submucosa. Radioautographs showed these 3H-5-HT binding sites to be in myenteric ganglia and in a broad unresolved band at the mucosal-submucosal interface. Antagonists active at receptors for other neurotransmitters than 5-HT, at either of the two known types of CNS 5-HT receptor, and at 5-HT uptake sites on serotonergic neurons failed to inhibit binding of 3H-5-HT. The structural requirements of analogues for binding to the enteric 5-HT receptor matched the known pharmacology of M or neural 5-HT receptors. A novel 5-HT antagonist was found. This compound, N-acetyl-5-hydroxytryptophyl-5-hydroxytryptophan amide (5-HTP-DP), antagonized the action of 5-HT on type II/AH cells of the myenteric plexus but did not affect the release or actions of acetylcholine (nicotinic or muscarinic) or substance P. 5-HTP-DP was also an equally potent displacer of 3H-5-HT from its binding sites on enteric membranes. It is concluded that the sites responsible for specific binding of 3H-5-HT are enteric M or neural 5-HT receptors. These receptors differ from those now known to be present in the CNS.

5-Hydroxytryptophan↗
PubMed1985

Heterogeneity of ganglia of the guinea pig myenteric plexus: an in vitro study of the origin of terminals within single ganglia using a covalently bound fluorescent retrograde tracer.

Experiments were done to test the hypothesis that individual ganglia of the myenteric plexus of the guinea pig small intestine are heterogeneous with respect to the location of the neurons that provide terminals to them. The myenteric plexus, attached to the longitudinal layer of smooth muscle, was maintained in vitro. Individual ganglia were injected with a variety of potential retrograde tracers by pressure microejection from the tip (20-micron diameter) of a glass micropipette. The fluorescent dye 4-acetoamido, 4'-isothiocyanostilbene-2,2'-disulphonic acid (SITS) was found to be an effective tracer, labeling neuronal perikarya, evidently by retrograde transport. SITS has previously been shown not to cross plasma membranes, but to be covalently bound to the outer surface of that membrane, and to be taken up by nerve terminals to be retrogradely transported to label neuronal cell bodies. SITS fluorescence was found in about 12% of the neurons within the ganglion into which it was injected and also in approximately ten times more neurons in discretely located distant ganglia. No labeling of neurons was found when SITS was injected into the bath or into the smooth muscle below the myenteric plexus. Damage to neural connectives obstructed the labeling of neurons in ganglia distal to the injection site. Individual SITS-injected myenteric ganglia were found to vary greatly in the ratios of intraganglionic SITS-labeled neurons to the total number of neurons within the injected ganglion. The ratios of the number of intraganglionic SITS-labeled neurons to SITS-labeled neurons in distant ganglia projecting to the injected ganglion from elsewhere in the myenteric plexus also varied greatly. More strikingly, individual ganglia differed over a wide range with respect to whether the neurons in distant ganglia that provided them with terminals were situated in the oral, anal, or circumferential direction. Although the majority of projections were found to be from orally located ganglia, individual ganglia were observed that received predominantly or exclusively anal or oral projections. Others received mixtures of terminals from ganglia that were anal, oral, or circumferential. This anatomical heterogeneity in the location of afferent inputs to individual myenteric ganglia is probably reflected in a functional heterogeneity as well and will have to be taken into account in further studies of the physiology of the myenteric plexus. Individual ganglia of the plexus can no longer be taken as anatomically and functionally equivalent to one another.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1985

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↗
PubMed1985

Physiological responses of guinea-pig myenteric neurons secondary to the release of endogenous serotonin by tryptamine.

Intracellular recordings showed that administration of pulses of tryptamine mimicked one of the actions of serotonin (a slow depolarization associated with an increased input resistance) on type II/AH neurons of the myenteric plexus. After superfusion at high concentration tryptamine initially acted like serotonin, but then blocked the action of serotonin on these cells. Measurements of the release of preloaded [3H]serotonin or [3H]norepinephrine revealed that tryptamine is a potent releaser of these labeled amines; this release is Ca2+ independent but temperature dependent. Moreover, incubation with tryptamine depleted the myenteric plexus of endogenous serotonin. Since tryptamine has previously been demonstrated not to inhibit the binding of [3H]serotonin to its enteric neural receptor we framed the hypothesis that the serotonin-releasing action of tryptamine is responsible for its ability to mimic serotonin when given in pulses or to desensitize serotonin receptors through the prolonged release of serotonin when it is superfused. This hypothesis was tested by examining the action of tryptamine on the serotonin-mediated slow excitatory postsynaptic potentials evoked in type II/AH neurons by fiber tract stimulation. Tryptamine superfusion antagonized these slow potentials as predicted. Moreover, after a long time when endogenous serotonin was depleted, the response of type II/AH neurons to exogenous serotonin recovered but the slow synaptic potential did not. The action of tryptamine on this neuron was relatively specific. When the slow synaptic potential and serotonin responses were blocked by tryptamine the type II/AH neurons still responded to acetylcholine. Fast excitatory postsynaptic potentials were not affected by tryptamine. Furthermore, other types of neurons (I/S) and other neuronal responses to serotonin (such as a fast depolarization with decreased input resistance or presynaptic inhibition of acetylcholine release) were not blocked by tryptamine. Finally, radioautographic studies revealed a neural uptake of tryptamine in the chemically sympathectomized myenteric plexus; however, the distribution of tryptamine in the plexus was different from that of serotonin and was not blocked by excess non-radioactive serotonin. Therefore tryptamine does not enter myenteric neurons via the specific serotonin uptake mechanism; however, zimelidine, found to be a selective inhibitor of the enteric uptake of serotonin, antagonized the release of serotonin by tryptamine and attenuated the effect of tryptamine on responses to serotonin.(ABSTRACT TRUNCATED AT 400 WORDS)

5-Methoxytryptamine↗
PubMed1985

Analysis of the Effect of Light and Temperature on the Fluence Response Curves for Germination of Rumex obtusifolius.

Both red light (10 minutes) and 35 degrees C treatment (60 minutes) stimulate the germination of seeds of Rumex obtusifolius otherwise maintained in darkness at 25 degrees C. Fluence response curves were determined for the effect of red light to stimulate germination of seeds with and without 35 degrees C treatment. The endogenous far-red absorbing form (Pfr) level in the seeds was determined using short saturating fluences of wavelengths of light which maintain different proportions of phytochrome as Pfr at equilibrium. In the seed batches investigated, the endogenous Pfr level was found to be 4% or less of the total phytochrome. High dark germination after 35 degrees C treatment does not result from an increase in sensitivity of the whole population to Pfr. Calculated fluence response curves for germination which best fit the experimental data suggest that seeds germinate in darkness after 35 degrees C treatment because of a nonphytochrome-related process (overriding factor).

Journal Article↗
PubMed1985

[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↗
PubMed1985

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↗
PubMed1985

Specific antagonism of enteric neural serotonin receptors by dipeptides of 5-hydroxytryptophan: evidence that serotonin is a mediator of slow synaptic excitation in the myenteric plexus.

Research on the role of serotonin (5-hydroxytryptamine, 5-HT) in the function of the enteric nervous system has been impeded by the lack of specific inhibitors of the enteric neural actions of 5-HT. Saturable, reversible, high affinity enteric binding sites for 3H-5-HT have recently been characterized and radioautographically located. Affinity for the 3H-5-HT binding site requires an indole ring substituted with a free hydroxyl group. These 3H-5-HT binding sites have been proposed to be enteric neural 5-HT receptors. This hypothesis was tested in the current study by comparing the ability of compounds to inhibit the binding of 3H-5-HT with their electrophysiologically determined actions on myenteric neurons. 5-Methoxytryptamine did not inhibit the binding of 3H-5-HT to enteric membranes and neither mimicked nor antagonized the effects of 5-HT on the membrane potential of myenteric neurons. Two dipeptides of 5-hydroxytryptophan, N-acetyl- and N-hexanoyl-5-hydroxytryptophyl-5-hydroxytryptophan amide (5-HTP-DP and N-hex-5-HTP-DP) inhibited the binding of 3H-5-HT (K1 = 0.25 microM for 5-HTP-DP and 1.19 microM for N-hex-5-HTP-DP). 5-HTP-DP applied by pressure microejection or superfusion (10 microM) antagonized the slow postsynaptic depolarization of myenteric neurons evoked by microejection of 5-HT. 5-HTP-DP also blocked the 5-HT-induced presynaptic reduction in amplitude of nicotinic fast synaptic potentials; however, 5-HTP-DP itself did not affect these responses. Moreover, 5-HTP-DP also failed to affect responses of myenteric neurons to microejected substance P, their muscarinic response to acetylcholine, or antidromic action potentials. In contrast, both dipeptides blocked the slow synaptic potentials seen in type II/AH neurons following stimulation of fiber tracts in interganglionic connectives. These data support the hypotheses that enteric 3H-5-HT binding sites are enteric neural 5-HT receptors, that dipeptides of 5-hydroxytryptophan are specific antagonists at these receptors, and that 5-HT is one of the mediators of slow synaptic potentials in the myenteric plexus.

5-Hydroxytryptophan↗
PubMed1984

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↗
PubMed1983

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↗
PubMed1981

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↗
PubMed1980

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↗
PubMed1979

[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↗