Modulation by C2 ceramide of the nicotinic transmission within the coeliac ganglion in the rabbit.

We have investigated the modulation by ceramide of the nicotinic activation of the prevertebral sympathetic neurons. Our study was performed in vitro in rabbit isolated coeliac ganglion, using intracellular recording techniques. We have used C(2) ceramide, a permeant analog of ceramide. The effects of C(2) ceramide were first assessed when nicotinic activation was elicited without modulatory mechanisms (fast excitatory postsynaptic potentials triggered by stimulation of the thoracic splanchnic nerves with a single pulse). In all the neurons tested, C(2) ceramide triggered an increase in the amplitude of the fast excitatory postsynaptic potentials demonstrating a direct facilitatory effect on the nicotinic activation. We then investigated the effects of C(2) ceramide on modulatory mechanisms of this activation. These mechanisms occur when a train of pulses of supramaximum intensity is applied on the splanchnic nerves. During the train, a gradual depression of fast nicotinic activation occurred: the pulses failed to systematically elicit action potentials. We have previously demonstrated that this regulatory phenomenon is partly modulated by nitric oxide which exerts a dual effect: facilitation or inhibition of the nicotinic activation. In all the neurons tested, C(2) ceramide decreased the number of action potentials fired during a train of pulses, demonstrating an indirect inhibitory effect on the nicotinic activation. The use of 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (nitric oxide scavenger) suppressed the inhibitory effect of C(2) ceramide, demonstrating that this effect is mediated through the nitric oxide pathway. C(2) dihydro-ceramide, an inactive analog of ceramide, was without effect on the nicotinic activation of the ganglionic neurons. These results demonstrate that ceramide exerts a complex modulation of the nicotinic activation of the prevertebral neurons: direct facilitation and indirect inhibition involving the nitric oxide pathway. In fact, C(2) ceramide plays a key gating role in the dual effect of the nitric oxide pathway by activating the inhibitory effect. The existence of this gating mechanism involving ceramide and nitric oxide opens new perspectives in terms of our understanding of the modulation of synaptic transmission within the prevertebral ganglia. Our study demonstrates that sphingolipids are involved in complex modulations of the synaptic activation within the prevertebral ganglia, and thus contribute to their integrative properties.

Effects of testosterone on the electrical properties and nicotinic transmission of the major pelvic and coeliac ganglion neurones.

The effects of testosterone on the electrical properties and nicotinic activation of prevertebral ganglion neurones were investigated in vitro on the male rat major pelvic ganglion and rabbit coeliac ganglion. The electrical activity of the neurones was recorded using intracellular recording techniques. Nicotinic activation was triggered for neurones of the major pelvic ganglion by stimulating the hypogastric, pelvic and cavernous nerves and for coeliac neurones by stimulating the splanchnic nerves. Testosterone modified the resting membrane potential of neurones in the major pelvic ganglion by triggering a slow depolarization, and was without significant effect on the resting membrane potential of coeliac ganglion neurones. In neurones of the major pelvic and coeliac ganglia, testosterone had no significant effect on the firing pattern, on the characteristics of the action potential (firing threshold, duration, overshoot) and on the after-hyperpolarization (amplitude and duration). Testosterone affected, in opposite ways, the nicotinic activation of neurones of the two prevertebral ganglia. In the major pelvic ganglion, testosterone triggered an increase in the amplitude of excitatory postsynaptic potentials induced by stimulation of the hypogastric, pelvic and cavernous nerves with a single pulse, revealing a facilitation of nicotinic activation. On coeliac ganglion neurones, testosterone elicited a decrease in the amplitude of excitatory postsynaptic potentials induced by stimulation of the splanchnic nerves, indicating an inhibition of nicotinic activation. Our study shows that testosterone acts differently on neurones of prevertebral ganglia involved in the nervous control of different functions, its facilitatory action being exerted on neurones of the major pelvic ganglion which is particularly involved in the control of the urogenital tract. Our study reinforces the concept, derived from neuroanatomical and pharmacological studies, of the major pelvic ganglion as a major peripheral target for testosterone.

Nitric oxide released by gastric mechanoreceptors modulates nicotinic activation of coeliac plexus neurons in the rabbit.

The effects on the nicotinic activation of the coeliac plexus neurons of nitric oxide (NO) released within the coeliac plexus by gastric mechanoreceptors, in particular during gastroduodenal inhibitory reflex, were assessed. This study was performed in the rabbit on an in vitro preparation of the coeliac plexus connected to the stomach and the duodenum. The electrical activity of ganglionic neurons was recorded with intracellular recording techniques. Water-filled balloons were used for gastric distensions and recording of duodenal motility. When a 10-s train of pulses (20-40Hz) of supramaximal intensity was applied to the splanchnic nerves, gradual depression of nicotinic activation occurred. Gastric distension (50 mL, 7.5 min) modulated this depression phenomenon by inhibiting or facilitating the nicotinic activation. In the neurons impaled during the recording of duodenal motility, gastric distension triggered an inhibition of nicotinic activation concomitantly with a gastroduodenal inhibitory reflex organized by the coeliac plexus. If the gastric distensions were performed while the coeliac plexus was superfused by a NO scavenger, the nicotinic activation was unaffected and the gastroduodenal inhibitory reflex was abolished. Moreover, when the coeliac plexus was superfused with an inhibitor of nitric oxide synthase, gastric distensions were without effect on the nicotinic activation. These results demonstrate that NO released within the coeliac plexus by gastric mechanoreceptors, in particular during the gastroduodenal inhibitory reflex, modulates the central nicotinic activation of coeliac plexus neurons, so NO released within a prevertebral ganglion by gastric afferent fibres, in particular during the organization by this ganglion of a reflex regulating the gastrointestinal tract motility, also exerts a gating of the central inputs to the ganglionic neurons.

Muscarinic receptor activation is a prerequisite for the endogenous release of nitric oxide modulating nicotinic transmission within the coeliac ganglion in the rabbit.

The aim of the present study was to investigate whether the activation of muscarinic receptors is a preliminary step to the endogenous release of nitric oxide modulating nicotinic transmission within the prevertebral ganglia. This work has been performed in vitro in isolated rabbit coeliac ganglion. The electrical activity of the ganglionic neurons was recorded using intracellular recording techniques. When a train of pulses of supramaximal intensity was applied to the splanchnic nerves, gradual depression of fast nicotinic transmission occurred: the pulses do not systematically elicit action potentials, but very often elicit excitatory postsynaptic potentials only. The use of pharmacological agents that interfere with the nitric oxide pathway such as L-arginine (precursor of nitric oxide) or 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (nitric oxide scavenger) demonstrated that nitric oxide modulates this depression phenomenon by facilitating or inhibiting the nicotinic transmission of the ganglionic neurons. A nitric oxide donor (diethylamine/nitric oxide complex) induced an inhibition of the nicotinic synaptic transmission. In the presence of the muscarinic receptors antagonist atropine, L-arginine and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide failed to modify the nicotinic transmission of the ganglionic neurons but diethylamine/nitric oxide complex was still able to inhibit it. These results demonstrate that in the coeliac ganglion, the activation of muscarinic cholinergic receptors is a prerequisite for the activation of neuronal nitric oxide synthase in preganglionic fibres. The nitric oxide released then exerts a facilitation or an inhibition of the nicotinic transmission of the ganglionic neurons. Atropine triggered a facilitation of the nicotinic transmission when superfused alone and an inhibition when superfused in the presence of 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. These results confirm that muscarinic receptors activate the nitric oxide pathway modulating the nicotinic transmission of the prevertebral neurons. Our results also demonstrate that when the nitric oxide pathway is blocked, activation of muscarinic receptors leads to facilitation of the nicotinic transmission. Our study brings new insights concerning the modulation by nitric oxide and by muscarinic receptors of the synaptic transmission within the prevertebral ganglia.

Release of nitric oxide within the coeliac plexus is involved in the organization of a gastroduodenal inhibitory reflex in the rabbit.

1. The coeliac plexus can organize a gastroduodenal inhibitory reflex without action potentials. The involvement of the nitric oxide-cGMP pathway in this reflex was investigated in the rabbit on an in vitro preparation of the coeliac plexus connected to the stomach and duodenum. Intraluminal duodenal pressures were measured with water-filled balloons. Gastric distension inhibited duodenal motility, thus characterizing a gastroduodenal inhibitory reflex organized by the coeliac plexus. 2. L-Arginine, superfused at the coeliac plexus level, enhanced this reflex, whereas Nomega-nitro-L-arginine (L-NOARG) or 2-(4-carboxyphenyl)-4,4,5,5 tetramethylimidazoline-1-oxyl-3-oxide (carboxy PTIO) reduced or abolished it. Moreover, diethylamine/nitric oxide complex superfused at the coeliac plexus level inhibited duodenal motility in the absence of gastric distension. 3. The effects of nitric oxide were mediated through the activation of guanylyl cyclase, as 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ) reduced or abolished the gastroduodenal inhibitory reflex, whereas zaprinast enhanced it. Moreover, 8-bromo-cGMP and cGMP, superfused at the coeliac plexus level, inhibited duodenal motility in the absence of gastric distension. 4. On the other hand, when perfused at the visceral level, L-NOARG, propranolol plus phentolamine, and guanethidine did not affect the reflex. Thus, neither nitric oxide nor noradrenaline could be the transmitters released at the muscular level to induce this reflex. 5. Our study demonstrates that the gastroduodenal inhibitory reflex, which is organized by the coeliac plexus without action potentials, is induced by the release within the plexus of nitric oxide acting on the cGMP pathway. These results provide new insights into the control of digestive motility by the prevertebral ganglia.

Integrative properties of the major pelvic ganglion in the rat.

The integrative properties of the major pelvic ganglion were investigated in the male rat on an in vitro preparation consisting of the ganglion connected to the hypogastric, pelvic and cavernous nerves. The electrical activity of ganglionic neurones was recorded using intracellular recording techniques. The neurones never displayed any spontaneous activity and were found to be only of the phasic type. Fast synaptic activation could be evoked in the same neurone by stimulating the hypogastric, pelvic and cavernous nerves with a single pulse. This activation was not affected by hexamethonium plus D-tubocurarine but was abolished by mecamylamine. During nerve stimulation with a train of pulses, a gradual depression of the fast synaptic responses occurred. This phenomenon increased with the frequency of stimulation. Our results show that the neurones of the major pelvic ganglion can integrate central inputs from both the sympathetic and parasympathetic systems as well as peripheral inputs. This activation is modulated by a rate limiting mechanism. Thus the major pelvic ganglion should not be considered as a simple relay but as a true integrative nervous centre which opens new perspectives concerning its role in the nervous control of the urogenital and gastrointestinal tracts.

Nerve-induced release of nitric oxide exerts dual effects on nicotinic transmission within the coeliac ganglion in the rabbit.

The involvement of nitric oxide in the modulation of nicotinic activation was investigated in vitro in isolated rabbit coeliac ganglion. The electrical activity of the ganglionic neurons was recorded using intracellular recording techniques. When a train of pulses of supramaximum intensity was applied to the splanchnic nerves, gradual depression of fast nicotinic activation occurred: the pulses do not systematically elicit action potentials, but very often elicit excitatory postsynaptic potentials only. This phenomenon appeared between 15 and 20 Hz and increased with the frequency of stimulation. It was not related to any change in the membrane potential of the ganglionic neurons. For a given frequency, the depression appeared progressively and it was particularly strong at the end of the train. The use of pharmacological agents that interfere with the nitric oxide pathway, such as L-arginine (precursor of nitric oxide), D-arginine (non-precursor of nitric oxide) N(omega_-nitro-L-arginine and N(omega)-nitro-L-arginine methyl ester (inhibitors of nitric oxide synthase), and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (nitric oxide scavenger), demonstrated that nitric oxide modulated this depression phenomenon by exerting a dual effect on the nicotinic activation, i.e. facilitation or inhibition. Agents interfering with the guanosine 3',5'-cyclic monophosphate pathway, such as oxadiazolo[4,3-a] quinoxalin-1-one (selective inhibitor of the nitric oxide-activated soluble guanylate cyclase) and zaprinast (selective inhibitor of the phosphodiesterases involved in the guanosine 3',5'-cyclic monophosphate pathway) demonstrated that only the facilitatory effect of nitric oxide on the nicotinic activation was mediated through the guanosine 3',5'-cyclic monophosphate pathway. The mechanism sustaining the inhibitory effect remains to be determined. By modulating the nicotinic activation, nitric oxide plays a role in the integrative properties of the prevertebral ganglia. This opens new perspectives with regard to the control of visceral functions by the prevertebral level of regulation.

The mammalian sympathetic prevertebral ganglia: integrative properties and role in the nervous control of digestive tract motility.

The prevertebral ganglia which are a constitutive part of the sympathetic system have long been considered as a simple relay on this efferent pathway. In fact, these ganglia must be considered as true peripheral nervous centres. They possess various integrative properties, such as projections of central and peripheral inputs onto the ganglionic neurones, gating of these projections and pacemaker activity of the ganglionic neurones. These properties explain the ability of these ganglia to participate in the regulation of various visceral functions, including digestive tract motility.

New insights into the organization of a gastroduodenal inhibitory reflex by the coeliac plexus.

The mechanisms involved at the prevertebral ganglionic level in a gastroduodenal inhibitory reflex were investigated in the rabbit on an in vitro preparation of the coeliac plexus connected to the stomach and duodenum. Intraluminal gastric and duodenal pressures were measured using water-filled balloons. Gastric distension inhibited duodenal motility via a nerve reflex which was abolished by section of the nerves connecting the coeliac plexus to the viscera. Superfusion of the coeliac plexus with a low Ca(2+)-high Mg2+ solution abolished the gastroduodenal inhibitory reflex, indicating a synaptic link at the ganglion level. The reflex was unaffected by superfusion of the coeliac plexus with hexamethonium and tubocurarine, ruling out a nicotinic mechanism. The reflex persisted when the coeliac plexus was superfused with tetrodotoxin or when the nerves connecting the coeliac plexus to the viscera were superfused with a Na(+)-free solution; these results indicate that the reflex does not involve sodium-dependent action potentials. Moreover, superfusion of the nerves connecting the coeliac plexus to the viscera with a calcium blocker or with a Ca(2+)-free solution also failed to abolish the reflex, suggesting that calcium-dependent action potentials are not involved. Our study demonstrates that a gastrointestinal inhibitory reflex via the coeliac ganglion is not based on fast synaptic inputs or action potentials. These results provide new insights concerning the physiology of the sympathetic prevertebral ganglia.

Involvement of a cholinergic mechanism in the sustained depolarization and contraction of the lower oesophageal sphincter muscle cells in the cat.

Membrane potentials were recorded in vitro with intracellular electrodes from the circular muscle cells of the cat lower oesophageal sphincter and oesophageal body. In addition, the tension of lower oesophageal sphincter and oesophageal body strips was recorded isotonically. Under the experimental conditions, no spontaneous electrical activity or variation in the tension of the strips occurred. The resting membrane potential of the circular muscle cells was significantly lower in the lower oesophageal sphincter (-51.0 +/- 0.3 mV) than in the circular muscle cells of the oesophageal body (-57.1 +/- 0.4 mV). These values were not affected by infusion of tetrodotoxin 3.1 x 10(-6) M. In the presence of atropine (3.5 x 10(-7) M), the resting membrane potential of the circular muscle cells of the lower oesophageal sphincter increased significantly (-57.6 +/- 0.4 mV), whereas the resting membrane potential of the circular muscle cells of the oesophageal body was not significantly affected (-57.8 +/- 0.6 mV). In the presence of atropine, no significant difference in the values of the resting membrane potential of the circular muscle cells was observed between the lower oesophageal sphincter and the oesophageal body. Hyoscine (2.9 x 10(-7) M) significantly increased the resting membrane potential of the circular muscle cells of the lower oesophageal sphincter, whereas eserine (3.6 x 10(-6) M) significantly decreased it. Atropine induced a significant decrease in the membrane resistance of the circular muscle cells of the lower oesophageal sphincter. Atropine decreased the resting tension of lower oesophageal sphincter strips whereas eserine increased it, but no such effects were recorded on oesophageal body strips.(ABSTRACT TRUNCATED AT 250 WORDS)

Modulation of synaptic transmission in the rabbit coeliac ganglia by gastric and duodenal mechanoreceptors.

The involvement of duodenal and gastric mechanoreceptors in the modulation of synaptic transmission was investigated in a rabbit sympathetic prevertebral ganglion. The present study was performed in vitro on the coeliac plexus connected to the stomach and the duodenum. The electrical activity of ganglionic neurons was recorded using intracellular recording techniques. The patterns of synaptic activation of these ganglionic neurons in response to the activation of mechanoreceptors by gastric or duodenal distension were investigated. Although gastric or duodenal distension was unable to elicit any fast synaptic activity in ganglionic neurons, it produced either an inhibition or a facilitation of the fast nicotinic excitatory postsynaptic potentials elicited by stimulation of the thoracic splanchnic nerves. In addition, this distension triggered long-lasting (3-11 min) modifications in the electrical properties of the ganglionic neurons, i.e. slow depolarizations (6-18 mV) or slow hyperpolarizations (3-6 mV), which were sometimes associated with a decrease in the input membrane resistance. After cooling of the nerves connecting the coeliac ganglia to the stomach, the activation of gastric or duodenal mechanoreceptors was no longer able to modify the fast synaptic activation or the electrical properties of the ganglionic neurons. The results demonstrate that gastric and duodenal mechanoreceptors project onto neurons of the coeliac ganglia and change their excitability as well as the central inputs they receive. The long duration of these modifications suggests that gastric and duodenal mechanoreceptors can modulate the activity of the neurons of the coeliac ganglia.

Non-cholinergic ascending excitatory response in the cat small intestine: possible involvement of substance P.

Using an electromyographic technique, an ascending excitatory response was recorded "in vitro" in the presence of atropine in the cat small intestine up to 70 mm orally with respect to the site of repetitive transmural nerve stimulation. This non-cholinergic ascending excitatory response was characterized by an increase in the slow wave amplitude and spiking activity. This response was reversibly abolished by Tetrodotoxin (3,1 X 10(-6) M) but remained unchanged after exposure of the intestine to: Hexamethonium (4,9 X 10(-6) M) plus Tubocurarine (1,4 X 10(-5) M), Guanethidine (5 X 10(-7) to 5 X 10(-5) M), Domperidone (2,3 X 10(-7) to 2,3 X 10(-5) M), Naloxone (3 X 10(-7) to 3 X 10(-5) M), Methysergide (2,8 X 10(-7) to 2,8 X 10(-5) M), Metergoline (2,4 X 10(-5) M), Methiotepin (2,1 X 10(-5) M) and Mepyramine (2,3 X 10(-5) M). This response was unaffected by the substance P analogues, D-Pro2, D-Phe7, D-Trp9-Substance P (10(-5) M) or D-Pro2, D-Trp7-9-Substance P (10(-5) M) but was reversibly abolished after exposure of the intestine to substance P (10(-6) M). Moreover substance P still effectively abolished this response in the presence of any two of the above analogues. The results of the present study show that the non-cholinergic excitatory response elicited in the cat small intestine due to the activity of long ascending pathways probably involved substance P. The functional significance of this response is discussed.

Enkephalins in the inferior mesenteric ganglion of the cat and in the area of the lower digestive tract innervated by this ganglion: quantification by radio-immunoassay and characterization by high pressure liquid chromatography.

Met-enkephalin, Leu-enkephalin and Met-enkephalin-Arg-Gly-Leu were quantified and characterized in the cat inferior mesenteric ganglion and in the area of the lower digestive tract innervated by this ganglion, including the proximal colon, distal colon and internal anal sphincter. In the structures studied, the concentrations of enkephalins expressed as femtomole/mg of wet tissue ranged from 66 to 160 with Met-enkephalin, from 15 to 45 with Leu-enkephalin and from 2 to 12 for Met-enkephalin-arg-gly-leu. In the lower digestive tract, the Met- and Leu-enkephalin content decreased from the proximal colon to the internal anal sphincter. The Met-enkephalin versus Leu-enkephalin ratio of the structures investigated were as follows: inferior mesenteric ganglion 3.2, proximal colon 4.4, distal colon 5, internal and sphincter 4.5. In individual samples of all the structures assayed the results of high pressure liquid chromatography (HPLC) analysis pointed to the presence of authentic Met- and Leu-enkephalin. HPLC analysis could not be carried out on Met-enkephalin-Arg-Gly-Leu due to the very low concentrations of this peptide in all the structures assayed. Our results, combined with those of previous immunohistochemical and physiological studies, support the idea that enkephalins are involved in the nervous control of the motility of the lower digestive tract.

Quantification and characterization of enkephalins in the upper part of the cat digestive tract and the coeliac ganglia.

The [Met]enkephalin, [Leu]enkephalin and [Met]enkephalin-arg-gly-leu contents of the upper part of the digestive tract (lower oesophageal sphincter, fundus, antrum, pylorus, duodenum, ileum) and coeliac ganglia of the cat were determined and identified. The enkephalin content of all the structures studied, expressed in femtomole/mg of wet tissue, was found to range from 83 to 446 with [Met]enkephalin; 19 to 63 with [Leu]enkephalin; 2.5 to 13 with [Met]enkephalin-arg-gly-leu. In the muscular and plexus layers the [Met]- and [Leu]enkephalin contents increase gradually from the lower oesophageal sphincter to the pylorus and then decrease from the duodenum to the ileum. The [Met]enkephalin versus [Leu]enkephalin ratio is 2.7 in the coeliac ganglia and ranges from 4.3 to 8.1 in the areas of the digestive tract investigated. In addition, the presence of authentic [Met]- and [Leu]enkephalin was confirmed in all the structures assayed by high pressure liquid chromatography. Owing to the low amounts of [Met]enkephalin-arg-gly-leu detected in individual samples of the coeliac ganglia and in the areas of the digestive tract investigated, it was not possible to characterize this peptide using high pressure liquid chromatography and therefore to confirm the presence of authentic [Met]enkephalin-arg-gly-leu in these structures. The differences in the enkephalin concentrations observed among these various areas of the digestive tract suggest that these peptides may act differently from one area to another, thus playing a complex integrative role in the nervous control of gastrointestinal tract motility.

Ascending responses induced by transmural nerve stimulation in the cat duodenum.

Electromyographic responses of the cat duodenum were recorded in vitro up to 5 cm oral to the site of transmural nerve stimulation. Repetitive stimulation induced ascending cholinergic and non-cholinergic excitatory responses characterized by an increase in the slow wave amplitude and spiking activity. Ascending inhibitory responses were also recorded and were characterized by a suppression of the spiking activity and a decrease in the slow wave amplitude. The ascending cholinergic excitatory response was abolished by atropine. The non-cholinergic excitatory and inhibitory responses both disappeared in the presence of tetrodotoxin.

The role of oesophageal and intestinal receptors in the control of gastric motility.

The aim of this work was to characterize the discharge pattern of vagal efferent fibers supplying the stomach, and the modifications of this pattern induced by stimulation of oesophageal or intestinal receptors. The experiments were performed on dogs in which the central end of the left thoracic vagus had been sutured to the peripheral end of the left phrenic nerve. In such preparations, the activity of the motor units of the reinnervated left hemidiaphragm indicated the activity of vagal efferent fibers. After the left hemidiaphragm had been transformed into subcutaneous muscle, it was possible to study, using electromyography, in the conscious dog, the discharge of efferent vagal fibers which originally supplied the stomach. All the gastric vagal efferent fibers presented a spontaneous discharge with a very low frequency (0.1 Hz less than f less than 5 Hz). The firing of some fibers was increased each time the gastric motility was enhanced: these fibers were considered to be excitatory fibers. In contrast, other fibers exhibited an opposite discharge pattern and they were considered to be inhibitory fibers. Among all the gastric fibers whose activity was recorded in this study, some of them presented a modification of discharge during the receptive relaxation of the proximal stomach produced by an oesophageal distension. The discharge of excitatory fibers was suppressed while that of the inhibitory fibers was markedly increased. Taking into account these modifications of discharge, parallel to the relaxation of the proximal stomach, it was assumed that these fibers originally supplied the gastric fundus.(ABSTRACT TRUNCATED AT 250 WORDS)

[Activity of vagal efferent fibres innervating the smooth muscle of the dog's cardia]. / Activité des fibres vagales efférentes destinées à la musculature lisse du cardia du chien.

Our experiments were performed on dogs in which the central end of the left thoracic vagus had been sutured to the peripheral end of the left phrenic nerve. In such preparations, the activity of motor units of the re-innervated left hemidiaphragm indicated the activity of the vagal efferent fibres. After the left hemidiaphragm had been transformed into subcutaneous muscle, we studied, (using electromyography in the unanesthetized dog), the discharge of vagal fibres which originally supplied the lower oesophageal sphincter (cardia). The present paper only deals with fibres showing low frequency tonic discharge. 1. For some fibres (VIC type ; N = 42), the spontaneous firing rate (1.5 less than f less than 4.5 spikes/s) is suddenly enhanced just after the buccopharyngeal stage of swallowing (12 less than f less than 16 spikes/s). The this discharge stops abruptly just before the end of oesophageal peristalsis and starts again 2 to 3 seconds later at a low frequency (15 less than f less than 4.5 spikes/s). 2. Other fibres (VEC ; N = 18), which also have a slow discharge frequency (1 less than f less than 3 spikes/s) stop firing soon after the onset of swallowing and remain silent until the end of oesophageal peristalsis. At this time, i.e. when the bolus enters the stomach, the discharge starts again with an increased frequency (5 less than mean frequency less than 9 spikes/s). 3. The behaviour of the tonic vagal fibres during swallowing, as well as their low discharge frequency, strongly suggest that these fibres originally controlled the smooth muscle of the lower oesophageal sphincter and excited either an inhibitory (VIC = vagal inhibitory fibres of cardia) or an excitatory control (VEC = vagal excitatory fibres of cardia) upon this area.