Equatorial currents in the Western Indian ocean.

Measurements were made in the equatorial Indian Ocean during spring and summer 1979 from the Somali coast to 62 degrees E in the interior of the western basin. The detailed vertical profiles of horizontal current show that the energetic dominance throughout the region of variability was on vertical scales of several hundreds of meters, confined to within a few degrees of the equator, as observed in 1976. The near-surface equatorial circulation responded directly to variations in the wind field, and satellite-tracked drifter buoys showed the equatorial surface jet extending across the width of the ocean. This eastward flow is generated by the eastward winds that appear in the interval between the northeast and southwest monsoons. The zonal velocity fluctuations extended in a consistent pattern over the observation region. The time and meridional scales of the variability were similar to those observed in 1976, suggesting that the velocity field is dominated by long-term, equatorially trapped motions with long zonal scales.

Controlling elements in a tribal maize from Colombia: fcu , a two-unit system.

The genetic basis for a striking aleurone color variegation of a maize population from Colombia is described. The variegation is the result of the interaction of a particular r allele, designated r-cu , and a specific factor, Fcu (Factor Cuna), that collectively compose a controlling element system. In the absence of Fcu, a variable dilute (nonvariegated) pigmentation is expressed in the aleurone. The degree of variegation is determined by differences in the dosage of the Fcu element; differences in variegation between kernels with one r-cu vs. two r-cu's cannot be detected. Because of the specificity of the interaction, Fcu is different from the three other well-known controlling elements, Dt, Ac and En(=Spm), and therefore represents a fourth controlling element system in maize. In addition to Fcu, the Cuna tribal maize contains two other controlling elements, Dt and a very weak En. The prevalence of controlling elements in natural maize populations is discussed.

Effects of enkephalins and morphine on spontaneous electrical activity and on junction potentials elicited by parasympathetic nerve stimulation in cat and rabbit colon.

1 The effects of Leu-enkephalin, Met-enkephalin and morphine on excitatory junction potentials (e.j.ps) and inhibitory junction potentials (i.j.ps) elicited by stimulation of efferent parasympathetic nerves were studied in cats and rabbits, anaesthetized and in vitro.2 Enkephalins (0.008 mg/kg in vivo and 10(-6)M in vitro) enhanced e.j.p. amplitude in rabbit proximal colon and decreased it in rabbit distal colon and in cat colon. Enkephalins decreased i.j.p. amplitude in all the three models.3 Morphine (0.2 mg/kg in vivo and 10(-6)M in vitro) had the same effects as enkephalins on e.j.ps. In contrast, morphine decreased i.j.p. amplitude in rabbit proximal and distal colon and increased it in cat colon.4 Enkephalins and morphine induced (especially in the cat) spike activity which was potentiated by atropine (0.1 mg/kg in vivo or 10(-6)M in vitro).5 All the effects of enkephalins and morphine were antagonized by naloxone (0.2 mg/kg in vivo or 10(-6)M in vitro).6 These results suggest that the facilitatory effects of enkephalins and morphine on e.j.ps of rabbit proximal colon are due to the absence of opiate receptors on the excitatory nerve pathway and to a removal of inhibition by blockade of the non-adrenergic, non-cholinergic inhibitory pathway. Enkephalinergic intramural neurones may modulate the activation of either excitatory or inhibitory pathways in intramural reflexes.

Radioautographic study of uptake and storage of indoleamines in the rabbit enterochromaffin cells.

After in vitro intra-arterial injection of tritium-labeled 5-hydroxytryptamine or -hydroxytryptophan ([3H]5-HT or [3H]5-HTP) (5 x 10(-7) M) in the presence of cold noradrenaline (5 x 10(-6) M) into rabbit colon, a clear-cut labeling pattern was observed by radioautography. Labelled cells were observed within the mucosa. The labeling was less important after [3H]5-HTP than after [3H]5-HT injection. Ultrastructural study indicates that labeling is confined to the cytoplasm and coincides with polymorphic secretory granules. Hence these labeled cells display not only APUD cells characteristics but also true neuronal properties.

Fenoverine: a novel synchronizer of smooth muscle motility by interference with cellular calcium flow.

Several in vivo and in vitro test models were used to study the mechanism of action of fenoverine, a novel synchronizer of smooth muscle motility. In vivo, the effects of fenoverine were tested in the rabbit proximal colon, recording its ability to modify the electromyographic activity, either spontaneous or electrically elicited, in the presence or absence of atropine. Fenoverine did not influence the spontaneous motility nor did it modify the effects of atropine, but it significantly reduced the contractions elicited by electrical stimulation. In vitro, isolated rabbit and rat colon and isolated rat myometrium were used. In rabbit colon, fenoverine failed to influence the spontaneous motility as well as the effects of atropine, while significantly inhibiting the electrically elicited excitatory junction potential. Fenoverine also significantly inhibited the isometric contractions induced in rat myometrium and colon by electrical stimulation, by depolarization with hyperpotassic solution, as well as those induced by acetylcholine in calcium-free/EGTA medium, with ID50 ranging from 8.10(-7) to 3.1.10(-6) M except in the isolated colon following K+ depolarization (5.10(-5) M), all actions compatible with a calcium-modulating mechanism. Based on the reported data, it is concluded that fenoverine does not act as a muscarinic or opiate-receptor antagonist, but that its main mechanism of action is due to modulation of the calcium gradient across the muscular cell membrane by regulating the influx of the extracellular calcium and/or the release of the intracellular pool.

Opposite effects of ecdysone and 20-hydroxyecdysone on in vitro uterus motility of a tsetse fly.

In order to examine the possible effects of ecdysteroids on parturition, we studied in vitro the influence of ecdysone and 20-hydroxyecdysone on the motility of isolated uterus from virgin and pregnant female tsetse fly (Glossina fuscipes). Ecdysone initiates phasic uterine contractions or enhances the frequency of preexisting contractile activity. In contrast, uterine contractions are decreased or abolished by 20-hydroxyecdysone. Pharmacological data indicate that tsetse fly uterus exhibits myogenic and nerve-evoked contractions. Ecdysteroids mainly act on nervous structures that control muscle contractions. Our results provide evidence for a specific action of ecdysteroids on a nerve-muscle target involved in female reproduction.

The physiological role of peripheral serotoninergic neurones. A review.

1. Serotoninergic neurones and neurones which takes up 5-hydroxytryptamine (5-HT) have been observed in sensory ganglia, but their physiological role remains unknown. 2. Serotoninergic neurones participating in the neural control of gut motility are present within the enteric intramural nervous system. 3. 5-HT applied to the serosa inhibits the peristaltic reflex in the small intestine. In contrast, peristalsis is stimulated by 5-HT applied to the serosa. 4. Intracellular microelectrode investigations indicate that some neurones of the enteric nervous system are depolarized, whereas others are hyperpolarized by 5-HT. In addition, 5-HT can also decrease the release of acetylcholine by acting on presynaptic receptors located on cholinergic nerve endings. The release of 5-HT from serotoninergic enteric neurones is very probably under the control of a noradrenergic mechanism. 5. Electromyographic studies on the rabbit colon indicate that a nerve-mediated descending inhibition is modified by drugs interacting with the synthesis of 5-HT or its reuptake.

Nervous control of the internal anal sphincter of the cat.

1. The effects of sympathetic and parasympathetic efferent nerve stimulation on the activity of longitudinal and circular coats of th anal sphincteric area have been studied on acute animals using extracellular electrical recordings. In addition, the effect of intramural sympathetic nerves stimulation has been investigated on anal sphincteric circular muscle, with the sucrose gap technique. 2. Hypogastric nerve stimulation elicited in anal sphincteric circular muscle slow time course depolarization responses (latency 200-400 msec) which were abolished by alpha-adrenergic blockers (dihydroergotamine, phentolamine). 3. Stimulation of the parasympathetic outflow to the internal anal sphincter (second ventral sacral root: VS2) inhibited spontaneous electrical activity of the circular muscle. Pharmacological arguments lead to the conclusion that the inhibition induced by VS2 stimulation is mediated through intramural non-adrenergic non-cholinergic (purinergic) inhibitory neurones. 4. Rectal distension caused an inhibition of the anal sphincteric circular muscle activity which persisted in the presence of atropine, phentolamine and propranolol, indicating that this inhibition was produced by non-adrenergic non-cholinergic intramural neurones. 5. VS2 stimulation produced only an activation of the longitudinal muscle of the sphincteric area, which was abolished by hexamethonium and atropine; in contrast, hypogastric nerve stimulation gave rise to an inhibition which was blocked by propranolol. These results indicate that the longitudinal muscle receives (1) an excitatory innervation from preganglionic parasympathetic nerves connected with intramural cholinergic neurones, and (2) an inhibitory sympathetic innervation from noradrenergic axons running in the hypogastric nerves. No inhibitory no-adrenergic non-cholinergic innervation was observed in the longitudinal muscle in response to VS2 stimulation. 6. The results obtained from simultaneous stimulation of VS2 and hypogastric nerves indicate that in the anal sphincteric circular muscle the release of noradrenaline from sympathetic nerves is modulated by cholinergic receptors located on noradrenergic nerve endings, muscarinic receptors which can abolish the release of noradrenaline, and probably nicotinic receptors which increase the noradrenaline release. The eventual functional significance of the nicotinic receptors is discussed.

Electrical activity from smooth muscle of the anal sphincteric area of the cat.

1. The electrical activities of longitudinal and circular smooth muscle of the anal sphincteric area have been studied in the cat. 2. Electromyographic recordings were achieved with extracellular electrodes, in vivo on acute and chronic animals, and in vitro on the isolated organ. In addition, electrical and mechanical activities were recorded from muscle strips with the sucrose gap technique. 3. Circular muscle coat electrical activity consisted exclusively of slow variations of the membrane potential of the smooth muscle cells. Each slow potential variation was followed by a contraction. 4. The electrical activity and the concomitant contractions were tetrodotoxin resistant (10(-6) g/ml.). Both disappeared in Ca-free solution or in the presence of Mn ions (10(-3) M). 5. On circular muscle, noradrenaline (10(-8)-10(-7) g/ml. in vitro, or 0.1-0.15 mg/kg in vivo) had an excitatory effect consisting in an increase of slow potential frequency. The action of noradrenaline was antagonized by phentolamine (10(-6)-10(-5) g/ml. in vitro, or 0.2 mg/kg in vivo). 6. On circular muscle, acetylcholine (10(-8)-10(-6) g/ml.), used exclusively on muscle strips, did never produce any clear cut effect. 7. Longitudinal muscle coat electrical activity consisted of spike potentials superimposed on slow time course depolarizations which were never observed alone. Each spike was followed by a contraction. This electrical activity was tetrodotoxin resistant (10(-6) g/ml.). 8. Longitudinal muscle activity was abolished by noradrenaline (10(-6) g/ml.) and enhanced by acetylcholine (10(-8)-10(-6) g/ml.). The action of noradrenaline was antagonized by propranolol (0.2 mg/kg I.V.; 10(-6) g/ml.) and that of acetylcholine by atropine (10(-7) g/ml.). 9. Electrophysiological and pharmacological data indicate that electromechanical coupling is achieved (1) in circular muscle, through Ca dependent slow variations in membrane potential of the muscle cells and (2) in longitudinal muscle, through spike potentials. Noradrenaline has opposite effects on the two muscle coats: circular muscle is excited through alpha-receptors located on muscle cells membrane; longitudinal muscle is inhibited through beta-receptors. Acetylcholine excites longitudinal muscle through muscarinic receptors, but it has no effect on circular muscle.

Role of M1 muscarinic receptors in the parasympathetic control of colonic motility in cats and rabbits.

1. The effects of pirenzepine (a selective blocking agent of M1 muscarinic receptors) were studied on excitatory junction potentials (EJPs) and inhibitory junction potentials (IJPs) elicited on colonic smooth muscle by stimulation of efferent parasympathetic nerve fibres in anaesthetized cats and rabbits. 2. Pirenzepine (25 micrograms kg-1 to 0.2 mg kg-1, i.v.) decreased the amplitude of EJPs or abolished them. In pirenzepine, parasympathetic stimulation elicited IJPs in most cases. 3. In both species, pirenzepine initiated spontaneous IJPs, indicating an increase in the activity of the non-adrenergic, non-cholinergic (NANC) inhibitory neurones. 4. The results suggest that M1 muscarinic receptors are involved in synaptic transmission within intramural plexuses, at interneuronal synapses in the parasympathetic excitatory pathway to colonic smooth muscle, but are not involved in the pathway to the NANC inhibitory neurones. The facilitation of IJPs by pirenzepine suggests that, under normal physiological conditions, NANC neurones are tonically inhibited by an intramural nervous circuit involving M1 muscarinic receptors.

Action of trimebutine in cat and rabbit colon: evidence of an opioid-like effect.

Because trimebutine (TMB) is a drug that modulates colonic motility, we have attempted to determine the modifications of electrical activity underlying the motor effects of this drug. Experiments have been carried out on cat colon in vivo and on rabbit proximal colon in vivo and in vitro. The action of TMB (0.5-2 mg/kg in vivo; 10(-7) M-10(-6) M in vitro) consisted of an initiation or of an increase of spike potential activity that was unaffected by atropine (0.1 mg/kg for the cat, 2-3 mg/kg in vivo and 10(-6) M in vitro for the rabbit) and by hexamethonium (1.5 mg/kg for the cat and 2 mg/kg in vivo or 10(-6) M in vitro for the rabbit). In the cat under atropine, spike activity became cyclical, i.e., bursts of spikes were interrupted by periods of electrical silence. In the cat, TMB decreased the amplitude of excitatory junction potentials. Under atropine, TMB induced rhythmic variations in the amplitude of inhibitory junction potentials for 30 to 40 min. In the rabbit under TMB, excitatory junction potentials were enhanced whereas inhibitory junction potential amplitude was decreased. All the effects of TMB on spontaneous activity as well as on junction potentials are very similar to those observed in a previous work with morphine and enkephalins. The effects of TMB, unaffected by guanethidine, were antagonized by naloxone (2 mg/kg in vivo, 10(-6) M in vitro). These results suggest that opiate receptors, presumably located on intramural neurons, are involved in the effects of TMB.(ABSTRACT TRUNCATED AT 250 WORDS)

Actions of morphine and enkephalins on the internal anal sphincter of the cat: relevance for the physiological role of opiates.

The effects of Leu-enkephalin, Met-enkephalin and morphine on the electrical activity of the internal anal sphincter were studied in anesthetized spinalized cats and in vitro on sphincteric muscle strips. All the effects of enkephalins and morphine were antagonized by naloxone (2 mg/kg, i.v. in vivo and 10(-6)M in vitro). In vivo, the enkephalins (0.01 mg/kg i.v.) and morphine (2 mg/kg, i.v.) decreased the amplitude of the excitatory responses evoked in the sphincter by stimulation of the hypogastric nerves. Opiates presumably act on the sympathetic nerve endings by reducing the release of noradrenaline. In vitro, the enkephalins (10(-6)M) and morphine (10(-6)M) had a similar inhibitory effect, indicating that opiates act, at least partly, at intramural level. In vivo, the enkephalins and morphine produced an inhibition of the spontaneous electrical activity of the internal anal sphincter. This inhibition occurs also in vitro; it is thus due to a peripheral effect of opiates acting either directly on the sphincteric smooth muscle cells, or through the nervous structures controlling sphincteric motility. In addition, the distribution of nerves containing enkephalin-like immunoreactivity, using whole mount preparations of cat internal anal sphincter, indicates that this area is supplied with a dense Leu- and Met-enkephalinergic innervation. Met- and Leu-enkephalin-like immunoreactive axons were detected within the circular and longitudinal muscles.

In vivo study of the role of muscarinic receptors in the parasympathetic control of rabbit colonic motility.

The aim of the present study was to elucidate the role of the non-M1 muscarinic receptors, in the extrinsic and intrinsic nerve control of in vivo colonic motility. Experiments were performed on the proximal colon of anaesthetized rabbits. In this species, the parasympathetic innervation of the proximal colon originates from the vagus nerves. The action of methoctramine and 4-diphenyl-acetoxy-N-methylpiperidine methobromide (4-DAMP) was studied on excitatory junction potentials (EJPs), and on inhibitory junction potentials (IJPs) elicited in smooth muscle cells by stimulating parasympathetic efferents. The effects of the same drugs on spontaneous spiking activity were also investigated. The EJPs either decreased or disappeared after intra-arterial (i.a.) administration of 4-DAMP (45 pg to 450 ng). In the presence of 4-DAMP, further intravenous (i.v.) administration of pirenzepine (0.1 mg.kg-1) had facilitatory effects on the inhibitory pathway, i.e., after abolition of the EJPs, vagal stimulation elicited IJPs. With the highest dose of 4-DAMP, vagal stimulation immediately elicited IJPs the amplitude of which still increased after pirenzepine. In the presence of 4-DAMP, the spontaneous spike discharge was not noticeably altered. Methoctramine (0.37 to 75 micrograms, i.a. or 50 micrograms to 0.2 mg.kg-1, i.v.) increased the amplitude of the EJPs, whereas it decreased that of the IJPs. In addition, at the same doses, it either initiated or increased spike discharges that were not altered by pirenzepine up to 0.2 mg.kg-1, i.v. The so-called rebound excitation occurring after IJPs was not affected by methoctramine. No change in the EJP or IJP amplitude was observed with gallamine at sufficiently high doses to paralyse striated muscles (up to 3 mg.kg-1.h-1). It is concluded that the parasympathetic excitatory pathway to smooth muscle is blocked by 4-DAMP, whereas it is facilitated by methoctramine. 4-DAMP has no effect on the inhibitory pathway which is strongly depressed by methoctramine; however, the fact that these two drugs have opposite effects indicates that 4-DAMP and methoctramine may act on different muscarinic receptor subtypes. In addition, the facilitatory effects of pirenzepine on IJPs observed in animals pre-treated with 4-DAMP, indicates that the latter drug may act on non-M1 and non-M2 (presumably M3) muscarinic receptors. Methoctramine acts on non-M1 and non-M3 (presumably M2) receptors. The spike discharge induced by methoctramine is presumably due to an increased release of acetylcholine, and possibly also of a non-cholinergic transmitter which has excitatory effects on smooth muscle, the identification of which requires further investigations.(ABSTRACT TRUNCATED AT 400 WORDS)

Role of vesical afferent nerve fibres involved in the control of internal anal sphincter motility.

The neural pathways involved in the interactions between urinary bladder and internal anal sphincter (IAS) were studied in anaesthetized spinal cats. Activation of vesical afferents produced in the IAS a reflex increase in the electrical activity and a reflex inhibition of the excitatory responses evoked by stimulation of one hypogastric nerve. Both reflexes are achieved partly in the lumbar spinal cord and partly within the inferior mesenteric ganglion.

Mechanism of the noradrenergic motor control on the lower oesophageal sphincter in the cat.

1. The release of labelled acetylcholine has been measured on lower oesophageal sphincter (l.o.s.) muscular strips previously loaded with tritiated choline. 2. This release was greatly increased by noradrenaline 10(-5) g/ml. and unaffected by atropine 10(-6) g/ml., but it was practically abolished if hemicholinium 5.2 X 10(-4) M was added to the incubating bath containing the tritiated choline. 3. A radioautographic study of sections of l.o.s. strips loaded with tritiated choline showed that the radioactivity was mainly located in the nervous cells of the enteric plexuses and that the muscular cells were very poorly labelled. 4. The increased release of acetylcholine induced by noradrenaline did not occur in a Ca2+-free or in a hypermagnesic Tyrode (12 mM). 5. Tetrodotoxin 10(-6) G/ml. had no effect on the increased release of acetylcholine induced by noradrenaline. In addition, sucrose gap recordings showed that the depolarizing effect of noradrenaline on l.o.s. muscular strips was unaffected by tetrodotoxin 10(-6) g/ml. 6. It is concluded that acetylcholine released in the l.o.s. under the action of noradrenaline originated from the synaptic endings of the cholinergic intramural neurones.