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N Clerc

Publications and source records attributed to N Clerc.

At least 19 recordsLinked to original sources
PubMed2005

Clinical and molecular genetic evaluation of patients with primary dystonia.

Primary dystonia is a movement disorder characterized by involuntary and sustained muscle contractions causing twisting or abnormal postures and mutations in several genes have been identified. Our goal was to investigate, whether the clinical presentation would differ between patients with a positive family history, and patients without. Furthermore, we have performed mutation analysis in the subgroup of patients with a positive family history. A total of 175 patients with primary dystonia were evaluated. Data on gender, presence and frequency of pain and tremor, age of onset, and the distribution of affected body parts were compared between patients with positive and negative family history. All exons of the torsion dystonia 1, GTP cyclohydrolase 1 and epsilon-sarcoglycan genes were examined in 40 patients by SSCP analysis of PCR products followed by sequencing of variant conformers. Dystonia patients with a positive family history of dystonia had an earlier age of onset and those with a positive family history of tremor more often associated tremor than those with a negative family history. Four new polymorphisms in the epsilon-sarcoglycan gene were found and others confirmed, but no known or new mutations could be detected. Our study supports the notion that primary dystonia is a genetically heterogeneous disease.

Adult↗
PubMed2004

Intrinsic primary afferent neurones of the digestive tract.

Intrinsic primary afferent neurones of the intestine are specialized neurones that encode information about the state of the intestine by transducing mechanical and chemical stimuli that reflect tension in the gut wall and the chemical nature of its contents. They connect with interneurones and motor neurones in the gut to form the circuits of intrinsic muscle motor, secretomotor and vasomotor reflexes. A large range of ionic currents occur in these neurones. The neurones have voltage-activated inward sodium currents (both tetrodotoxin-sensitive and tetrodotoxin-insensitive) and inward calcium currents. Calcium entering during the action potential activates a slow after hyperpolarizing potassium current that has a profound influence on subsequent action potential firing. They also exhibit a prominent hyperpolarization-activated nonspecific cation current. The excitability of these neurones and sensory transduction are altered when the gut is inflamed. Changed excitability can persist after the inflammatory state has subsided. Intrinsic primary afferent neurones are thus important, both to the normal physiology and to pathophysiology of the small and large intestines.

Action Potentials↗
PubMed2003

Neuronal location of 5-hydroxytryptamine3 receptor-like immunoreactivity in the rat colon.

The presence of 5-hydroxytryptamine(3) receptors on enteric neurons is known from pharmacological data that date back more than 40 years. However, an adequate account of which neurons bear these receptors has not been made because suitable antisera have not been available. We have found that the majority of antisera that have been raised against sequences from the 5-hydroxytryptamine(3) receptor also recognize pre-prosomatostatin. We report that this source of false labeling can be eliminated by pre-incubating the antisera with a peptide designed for this purpose. We have used the pre-absorbed antiserum to localize 5-hydroxytryptamine(3) receptors in the rat colon. Immunoreactive nerve cell bodies occurred in the myenteric and submucosal ganglia. The majority had smooth cell bodies and long, smooth processes, that is, Dogiel type II morphology. The initial segments of the long processes of the Dogiel type II neurons were strongly immunoreactive. About 12% of immunoreactive myenteric nerve cells were of the same or smaller size, and had multiple short filamentous processes. Some of the immunoreactive Dogiel type II neurons were also immunoreactive for calretinin in both plexuses, and the majority were immunoreactive for calbindin in submucosal ganglia. Specific immunoreactivity occurred in non-varicose, but not in varicose, fibers in the myenteric and submucosal ganglia, and in fiber bundles that traversed the longitudinal and circular muscle layers. Immunoreactive varicose fibers were observed only in the mucosa. It is concluded that 5-hydroxytryptamine(3) receptors occur on intrinsic sensory neurons in the rat colon, and on extrinsic sensory nerve fibers that innervate the colon.

Animals↗
PubMed2002

Neurokinin-1 and neurokinin-3 receptors are expressed in vagal efferent neurons that innervate different parts of the gastro-intestinal tract.

Vagal efferent neurons innervating the digestive tract are mainly contained in the dorsal motor nucleus of the vagus. Previous studies have suggested that neurokinins and their neurokinin-1 and neurokinin-3 receptors are involved in the parasympathetic control of digestive functions. The purpose of the present study was to analyze the distribution of neurokinin-1 and neurokinin-3 receptors amongst vagal efferent neurons innervating the stomach, the duodenum, the ileum and the cecum. The immunocytochemical detection of neurokinin-1 and neurokinin-3 receptors was combined with the immunocytochemical detection of retrogradely transported cholera toxin-B subunit, previously injected in the gut wall. Neurokinin-1 and neurokinin-3 receptors were present in 19+/-7% and 8+/-3% of retrogradely labeled neurons innervating the stomach. Almost half of the labeled neurons innervating the duodenum (46+/-7%) expressed neurokinin-1 receptors but less than 0.5% contained neurokinin-3 receptors. None of the retrogradely labeled vagal efferent neurons innervating the ileum and the cecum were immunoreactive for neurokinin-1 and neurokinin-3 receptors. We conclude that neurokinin-1 and neurokinin-3 receptors are located on vagal efferent neurons which innervate the stomach and that neurokinin-1 receptors are common, whereas neurokinin-3 receptors are rare on neurons projecting to the duodenum. Additionally, the distal part of the rat small intestine is innervated by vagal efferent neurons that do not express neurokinins receptors on their membrane. This suggests that neurokinins may influence the parasympathetic control of different regions of the gastro-intestinal tract in specific ways.

Animals↗
PubMed2002

Responses of myenteric S neurones to low frequency stimulation of their synaptic inputs.

Previous experiments have shown that prolonged low frequency stimulation of presynaptic inputs causes excitation of AH neurones that considerably outlasts the period of stimulation in the guinea-pig small intestine. The present experiments compare the responses of S neurones (which are motor neurones and interneurones) with responses of AH neurones (intrinsic primary afferent neurones) to low frequency stimulation of synaptic inputs. Neurones in the myenteric plexus of isolated segments of guinea-pig small intestine were recorded from with intracellular microelectrodes. During their impalement, the neurones were filled with a marker dye and they were later processed to reveal their shapes and immunohistochemical properties. One group of neurones, inhibitory motor neurones to the circular muscle, was depolarised by stimulation of synaptic inputs at 1 Hz for 100 s to 4 min. With 4-min trains of stimuli, peak depolarisation was 21+/-2 mV (mean+/-S.E.M.), which was reached at about 110 s. Depolarisation was accompanied by increased excitability; before stimulation, a test intracellular pulse (500 ms) triggered 3 action potentials, at the peak of excitability this reached 16 action potentials. Depolarisation began to decline immediately at the end of stimulation. This contrasts with responses of AH neurones, in which depolarisation persisted after the end of the stimulus (peak depolarisation at 300 s). The excitation and depolarisation of inhibitory motor neurones was blocked by the neurokinin 1 tachykinin receptor antagonist, SR140333 (100 nM), but excitation of AH neurones was not affected. Small or no responses to 1 Hz stimulation were recorded from descending filamentous interneurones, longitudinal muscle motor neurones and excitatory circular muscle motor neurones. In conclusion, this study indicates that sustained slow postsynaptic excitation only occurs in AH neurones, and that one type of S neurones, inhibitory motor neurones to the circular muscle, responds substantially, but not beyond the period of stimulation, to activation of synaptic inputs at 1 Hz. This slow excitatory postsynaptic potential evoked by low frequency stimulation is mediated by tachykinins.

Action Potentials↗
PubMed2001

Effects of vagal and splanchnic section on food intake, weight, serum leptin and hypothalamic neuropeptide Y in rat.

Truncal vagotomy can cause reduced food intake and weight loss in humans and laboratory animals. In order to investigate some of the factors that might contribute to this effect, we studied changes in ingestive behaviour, whole body and organ weights, serum leptin and hypothalamic neuropeptide Y in rats with bilateral vagal section, bilateral splanchnic nerve section and combined vagotomy plus splanchnectomy. Pyloromyotomy was combined with vagotomy to lessen effects of vagotomy on gastric emptying. Animals with vagotomy or vagotomy plus splanchnectomy lost weight and decreased their daily food intake relative to animals with splanchnectomy alone, rats with bilateral sham exposure of one or both nerve, or rats with pyloromyotomy alone. Serum leptin and white fat mass, 4 weeks after vagotomy, were about 20% of the values in the sham-operated animals at this time. No effect for splanchnic nerve section alone was observed. Pyloromyotomy caused no reduction in weight or fat mass, but reduced serum leptin. Following vagotomy with or without splanchnic nerve section, neuropeptide Y was elevated in the arcuate nucleus relative to values for the other four groups. Changes in neuropeptide Y were inversely correlated with levels of serum leptin. It is concluded that the effect of vagotomy could be due to the loss of a feeding signal carried by vagal afferent neurons, or to changed humoral signals, for example, increased production of a satiety hormone. However, it cannot be attributed to signals that reduce feeding (for example, gastric distension) reaching the central nervous system via the splanchnic nerves. The changes were sufficient to cause weight loss even though serum leptin was decreased, a change that would be expected to increase food intake.

Adipose Tissue↗
PubMed2001

Comparison of the effects of neurokinin-3 receptor blockade on two forms of slow synaptic transmission in myenteric AH neurons.

AH neurons are intrinsic sensory neurons of the intestine that exhibit two types of slow synaptic event: slow excitatory postsynaptic potentials which increase their excitability for about 2-4 min, and sustained slow postsynaptic excitation which can persist for several hours, and may be involved in long-term changes in the sensitivity of the intestine to sensory stimuli. The effects of the neurokinin-3 tachykinin receptor antagonist, SR142801, on these two types of synaptic event in AH neurons of the myenteric ganglia of guinea-pig small intestine were compared. Slow excitatory postsynaptic potentials were evoked by stimulation of synaptic inputs at 10-20 Hz for 1s, and sustained slow postsynaptic excitation was evoked by stimulation of inputs at 1Hz for 4 min. SR142801 (1microM) reduced the amplitude of the slow excitatory postsynaptic potential to 26% of control, and also reduced the increase in input resistance and the extent of anode break excitation associated with the slow excitatory postsynaptic potential. In contrast, SR142801 did not reduce the increase in excitability, the increase in input resistance or the depolarisation that occur during the sustained slow postsynaptic excitation. SR142801 did not change the resting membrane potential or the resting input resistance. We conclude that tachykinins, acting through neurokinin-3 receptors, are involved in the generation of the slow excitatory postsynaptic potential, but not in the sustained slow postsynaptic excitation, and that the release of transmitters from synaptic inputs to AH neurons is frequency coded.

Action Potentials↗
PubMed2000

The soma and neurites of primary afferent neurons in the guinea-pig intestine respond differentially to deformation.

1. Intrinsic primary afferent neurons in the small intestine are exposed to distortion of their processes and of their cell bodies. Recordings of mechanosensitivity have previously been made from these neurons using intracellular microelectrodes, but this form of recording has not permitted detection of generator potentials from the processes, or of responses to cell body distortion. 2. We have developed a technique to record from enteric neurons in situ using patch electrodes. The mechanical stability of the patch recordings has allowed recording in cell-attached and whole cell configuration during imposed movement of the neurons. 3. Pressing with a fine probe initiated generator potentials (14 +/- 9 mV) from circumscribed regions of the neuron processes within the same myenteric ganglion, at distances from 100 to 500 microm from the cell body that was patched. Generator potentials persisted when synaptic transmission was blocked with high Mg2+, low Ca2+ solution. 4. Soma distortion, by pressing down with the whole cell recording electrode, inhibited action potential firing. Consistent with this, moderate intra-electrode pressure (10 mbar; 1 kPa) increased the opening probability of large-conductance (BK) potassium channels, recorded in cell-attached mode, but suction was not effective. In outside-out patches, suction, but not pressure, increased channel opening probability. Mechanosensitive BK channels have not been identified on other neurons. 5. The BK channels had conductances of 195 +/- 25 pS. Open probability was increased by depolarization, with a half-maximum activation at a patch potential of 20 mV and a slope factor of 10 mV. Channel activity was blocked by charybdotoxin (20 nM). 6. Stretch that increased membrane area under the electrode by 15 % was sufficient to double open probability. Similar changes in membrane area occur when the intestine changes diameter and wall tension under physiological conditions. Thus, the intestinal intrinsic primary afferent neurons are detectors of neurite distortion and of compression of the soma, these stimuli having opposite effects on neuron excitability.

Action Potentials↗
PubMed2000

Ultrastructural analysis of spinal primary afferent fibers within the circular muscle of the cat lower esophageal sphincter.

We have analyzed the ultrastructural characteristics and environment of spinal primary afferent fibers that run within the circular muscle of the cat lower esophageal sphincter. These were selectively labeled by anterogradely transported cholera toxin B subunit conjugated with horseradish peroxidase. Most of the labeled fibers were perpendicular to the muscle cells but some ran sinuously or parallel to the muscle cells. All the labeled fibers were unmyelinated and exhibited relatively rare varicosities. Most of the fibers were in large nerve fiber bundles surrounded by perineurium and probably project to the mucosa. Only some fibers that were in small nerve fiber bundles with no perineurium ran parallel to the musculature and established close relationships with smooth muscle cells. They might be a small subpopulation of the spinal tension receptors, most of the other spinal tension receptors being located in the myenteric plexus area, between the circular and longitudinal muscle.

Animals↗
PubMed2000

Shapes and projections of tertiary plexus neurons of the guinea-pig small intestine.

The axons of neurons that innervate the longitudinal muscle of the small intestine in small mammals such as rabbit, rat, guinea pig and mouse form a network, the tertiary plexus, against the inner surface of the muscle. In general, because of their substantial overlap, it has not been possible to follow the ramifications of individual axons in the tertiary plexus. In the present work, the longitudinal muscle motor neurons were filled with marker dyes through an intracellular microelectrode, and their morphologies and projections were examined in whole-mount preparations of longitudinal muscle and myenteric plexus. Most neurons that were examined were in the small intestine (ileum and duodenum), but a few were examined in the distal colon. Neurons in all regions had similar morphologies and projections. The cell bodies were amongst the smallest in myenteric ganglia, with major and minor axes of 14 microns and 25 microns (mean, n = 40) in the plane of the myenteric plexus. Each neuron had a single axon that branched extensively in the tertiary plexus, most had multiple lamellar dendrites and a few had filamentous dendrites or a mixture of filamentous and lamellar dendrites. The mean area of muscle covered by an axon and its branches extended 1.6 mm orally to anally and 1.7 mm circumferentially. The area covered was 2.8 +/- 1.9 mm2 (mean +/- SD, n = 23). From the density of occurrence of cell bodies, it can be calculated that each point in the longitudinal muscle is innervated by the processes of about 100 motor neurons and is influenced by electrotonic conduction of signals through the muscle by about 300 motor neurons.

Animals↗
PubMed1999

Contractile activity in intestinal muscle evokes action potential discharge in guinea-pig myenteric neurons.

1. The process by which stretch of the external muscle of the intestine leads to excitation of myenteric neurons was investigated by intracellular recording from neurons in isolated longitudinal muscle-myenteric plexus preparations from the guinea-pig. 2. Intestinal muscle that was stretched by 40 % beyond its resting size in either the longitudinal or circular direction contracted irregularly. Both multipolar, Dogiel type II, neurons and uniaxonal neurons generated action potentials in stretched tissue. Action potentials persisted when the membrane potential was hyperpolarized by passing current through the recording electrode for 10 of 14 Dogiel type II neurons and 1 of 18 uniaxonal neurons, indicating that the action potentials originated in the processes of these neurons. For the remaining four Dogiel type II and 17 uniaxonal neurons, the action potentials were abolished, suggesting that they were the result of synaptic activation of the cell bodies. 3. Neurons did not fire action potentials when the muscle was paralysed by nicardipine (3 microM), even when the preparations were simultaneously stretched by 50 % beyond resting length in longitudinal and circular directions. Spontaneous action potentials were not recorded in unstretched (slack) tissue, but when the L-type calcium channel agonist (-)-Bay K 8644 (1 microM) was added, the muscle contracted and action potentials were observed in Dogiel type II neurons and uniaxonal neurons. 4. The proteolytic enzyme dispase (1 mg ml-1) added to preparations that were stretched 40 % beyond slack width caused the myenteric plexus to lift away from the muscle, but did not prevent muscle contraction. In the presence of dispase, the neurons ceased firing action potentials spontaneously, although action potentials could still be evoked by intracellular current pulses. After the action of dispase, (-)-Bay K 8644 (1 microM) contracted the muscle but did not cause neurons to fire action potentials. 5. Gadolinium ions (1 microM), which block some stretch activated ion channels, stopped muscle contraction and prevented action potential firing in tissue stretched by 40 %. However, when (-)-Bay K 8644 (1 microM) was added in the presence of gadolinium, the muscle again contracted and action potentials were recorded from myenteric neurons. 6. Stretching the tissue 40 % beyond its slack width caused action potential firing in preparations that had been extrinsically denervated and in which time had been allowed for the cut axons to degenerate. 7. The present results lead to the following hypotheses. The neural response to stretching depends on the opening of stretch activated channels in the muscle, muscle contraction in response to this opening, and mechanical communication from the contracting muscle to myenteric neurons. Distortion of sensitive sites in the processes of the neurons opens channels to initiate action potentials that are propagated to the soma, where they are recorded. Neurons are also excited indirectly by slow synaptic transmission from neurons that respond directly to distortion.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1999

Long-term effects of synaptic activation at low frequency on excitability of myenteric AH neurons.

Intracellular microelectrodes were used to record the effects of extended periods (1-30 min) of synaptic activation on AH neurons in the myenteric ganglia of the guinea-pig ileum. Low-frequency (1 Hz) stimulation gave rise to a slowly developing, sustained increase in excitability of the neurons associated with depolarization and increased input resistance. The increased excitability lasted for up to 3.5 h following the stimulus period. Successive stimulus trains (1-4 min) elicited successively greater increases in excitability. The neurons went through stages of excitation. Before stimulation, 500-ms depolarizing pulses evoked up to three action potentials (phasic response) and anode break action potentials were not observed. As excitability increased, more action potentials were evoked by depolarization (the responses became tonic), anode break action potentials were observed, prolonged after hyperpolarizing potentials that follow multiple action potentials were diminished and, with substantial depolarization of the neurons, invasion by antidromic action potentials was suppressed. It is concluded that a state of elevated excitability is induced in myenteric AH neurons by synaptic activation at low frequency and that changes in excitability can outlast stimulation by several hours.

Action Potentials↗
PubMed1999

Nutrient tasting and signaling mechanisms in the gut. II. The intestine as a sensory organ: neural, endocrine, and immune responses.

The lining of the gastrointestinal tract is the largest vulnerable surface that faces the external environment. Just as the other large external surface, the skin, is regarded as a sensory organ, so should the intestinal mucosa. In fact, the mucosa has three types of detectors: neurons, endocrine cells, and immune cells. The mucosa is in immediate contact with the intestinal contents so that nutrients can be efficiently absorbed, and, at the same time, it protects against the intrusion of harmful entities, such as toxins and bacteria, that may enter the digestive system with food. Signals are sent locally to control motility, secretion, tissue defense, and vascular perfusion; to other digestive organs, for example, to the stomach, gallbladder, and pancreas; and to the central nervous system, for example to influence feeding behavior. The three detecting systems in the intestine are more extensive than those of any other organ: the enteric nervous system contains on the order of 10(8) neurons, the gastroenteropancreatic endocrine system uses more than 20 identified hormones, and the gut immune system has 70- 80% of the body's immune cells. The gastrointestinal tract has an integrated response to changes in its luminal contents. When this response is maladjusted or is overwhelmed, the consequences can be severe, as in cholera intoxication, or debilitating, as in irritable bowel syndrome. Thus it is essential to obtain a full understanding of the sensory functions of the intestine, of how the body reacts to the information, and of how neural, hormonal, and immune signals interact.

Animals↗
PubMed1998

Intrinsic primary afferent neurons of the intestine.

After a long period of inconclusive observations, the intrinsic primary afferent neurons of the intestine have been identified. The intestine is thus equipped with two groups of afferent neurons, those with cell bodies in cranial and dorsal root ganglia, and these recently identified afferent neurons with cell bodies in the wall of the intestine. The first, tentative, identification of intrinsic primary afferent neurons was by their morphology, which is type II in the terminology of Dogiel. These are multipolar neurons, with some axons that project to other nerve cells in the intestine and other axons that project to the mucosa. Definitive identification came only recently when action potentials were recorded intracellularly from Dogiel type II neurons in response to chemicals applied to the lumenal surface of the intestine and in response to tension in the muscle. These action potentials persisted after all synaptic transmission was blocked, proving the Dogiel type II neurons to be primary afferent neurons. Less direct evidence indicates that intrinsic primary afferent neurons that respond to mechanical stimulation of the mucosal lining are also Dogiel type II neurons. Electrophysiologically, the Dogiel type II neurons are referred to as AH neurons. They exhibit broad action potentials that are followed by early and late afterhyperpolarizing potentials. The intrinsic primary afferent neurons connect with each other at synapses where they transmit via slow excitatory postsynaptic potentials, that last for tens of seconds. Thus the intrinsic primary afferent neurons form self-reinforcing networks. The slow excitatory postsynaptic potentials counteract the late afterhyperpolarizing potentials, thereby increasing the period during which the cells can fire action potentials at high rates. Intrinsic primary afferent neurons transmit to second order neurons (interneurons and motor neurons) via both slow and fast excitatory postsynaptic potentials. Excitation of the intrinsic primary afferent neurons by lumenal chemicals or mechanical stimulation of the mucosa appears to be indirect, via the release of active compounds from endocrine cells in the epithelium. Stretch-induced activation of the intrinsic primary afferent neurons is at least partly dependent on tension generation in smooth muscle, that is itself sensitive to stretch. The intrinsic primary afferent neurons of the intestine are the only vertebrate primary afferent neurons so far identified with cell bodies in a peripheral organ. They are multipolar and receive synapses on their cell bodies, unlike cranial and spinal primary afferent neurons. They communicate with each other via slow excitatory synaptic potentials in self reinforcing networks and with interneurons and motor neurons via both fast and slow EPSPs.

Animals↗
PubMed1998

Correlation of electrophysiological and morphological characteristics of myenteric neurons of the duodenum in the guinea-pig.

Intracellular recording, dye filling and immunohistochemistry were used to investigate neurons of the proximal duodenum of the guinea-pig. Recordings were made from neurons of the myenteric plexus in the presence of nicardipine to quell muscle contractions, using microelectrodes that contained the marker substance Neurobiotin. Preparations were subsequently processed histochemically to reveal nerve cell shapes and immunoreactivity for calbindin, calretinin or nitric oxide synthase. Neurons were distinguished by their shapes and axonal projections as Dogiel type II, Dogiel type I, filamentous descending interneurons and small filamentous neurons. Dogiel type II cells had large cell bodies and multiple axon processes. They each had a broad action potential (mean half-width, 2.9 ms) and a prominent inflection (hump) on the falling phase of the action potential. The majority (70%) of Dogiel type II cells were AH neurons, defined by their having a prolonged hyperpolarizing potential that followed a soma action potential and lasted more than 2 s. Fast excitatory postsynaptic potentials were not recorded from Dogiel type II neurons. Two thirds of Dogiel type II neurons fired phasically in response to intracellularly injected 500 ms depolarizing current pulses and one-third fired tonically. Calbindin immunoreactivity occurred in 70% of Dogiel type II neurons. Dogiel type I neurons had lamellar dendrites and a single axon. They had brief action potentials (mean half-width, 1.7 ms) with no, or a slight hump. They responded to fibre tract stimulation with fast excitatory postsynaptic potentials. Only 2/21 exhibited a prolonged hyperpolarization following action potentials. The majority of Dogiel type I neurons thus belong to the S neuron category. Nine Dogiel type I neurons fired phasically in response to 500 ms depolarizing current pulses, while 12 fired tonically. Filamentous descending interneurons had long, branching filamentous dendrites and a single anally-projecting axon which gave rise to varicose branches in myenteric ganglia. Action potential characteristics of filamentous interneurons ranged between those of Dogiel type II and type I neurons. Small neurons. Small neurons with short filamentous, or few simple dendrites were also characterized. They had single axons, which could be traced either locally to the circular muscle, or to the longitudinal muscle. None of 12 filamentous interneurons or of 10 small filamentous neurons exhibited a prolonged post-spike hyperpolarization, whereas fast excitatory postsynaptic potentials were recorded from a majority. It is concluded that the morphological types of neuron that are encountered in the ileum also occur in the duodenum, but the electrophysiological characteristics of the neurons are more variable for each morphological class. Thus, it is not always possible to predict the morphology of myenteric neurons in the duodenum from their electrophysiological properties. Part of the electrophysiological variability appears to be due to duodenal neurons being more excitable than ileal neurons.

Action Potentials↗
PubMed1998

Morphological and immunohistochemical identification of neurons and their targets in the guinea-pig duodenum.

Nerve circuits within the proximal duodenum were investigated using a combination of immunohistochemistry for individual neuron markers and lesion of intrinsic nerve pathways to determine axon projections. Cell shapes and axonal projections were also studied in cells that had been injected with a marker substance. Several major neuron populations were identified. Calbindin immunoreactivity occurred in a population of myenteric nerve cells with Dogiel type II morphology. These had axons that projected to other myenteric ganglia, to the circular muscle and to the mucosa. All were immunoreactive for the synthesizing enzyme for acetylcholine, choline acetyltransferase, and some were also immunoreactive for calretinin. Myenteric neurons with nitric oxide synthase immunoreactivity projected anally to the circular muscle. These were also immunoreactive for vasoactive intestinal peptide, and proportions of them had enkephalin and/or neuropeptide Y immunoreactivity. It is suggested that they are inhibitory motor neurons to the circular muscle. A very few (about 2%) of nitric oxide synthase-immunoreactive neurons had choline acetyltransferase immunoreactivity. Tachykinin (substance P)-immunoreactive nerve cells were numerous in the myenteric plexus. Some of these projected orally to the circular muscle and are concluded to be excitatory motor neurons. Others projected to the tertiary plexus which innervates the longitudinal muscle and others provided terminals in the myenteric plexus. Two groups of descending interneurons were identified, one with somatostatin immunoreactivity and one with vasoactive intestinal peptide immunoreactivity. The two most common nerve cells in submucous ganglia were neuropeptide Y- and vasoactive intestinal peptide-immunoreactive nerve cells. Both provided innervation of the mucosa. There was also a population of calretinin-immunoreactive submucous neurons that innervated the mucosal glands, but not the villi. Comparison with the ileum reveals similarities in the chemistries and projections of neurons. Differences include the almost complete absence of nitric oxide synthase immunoreactivity from vasoactive intestinal peptide-immunoreactive interneurons in the duodenum, the projection of calbindin-immunoreactive Dogiel type II neurons to the circular muscle and the absence of tachykinin-immunoreactivity from these neurons.

Animals↗