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At least 757 records · Page 42Linked to original sources
PubMed1991

Characterization of somatodendritic neuronal nicotinic receptors located on the myenteric plexus.

The effects of nicotine and dimethylphenylpiperazinium (DMPP) on resting and stimulation-evoked release of [3H]-acetylcholine ([3H]ACh) from cholinergic interneurons and neuro-effector neurons of the ileal longitudinal muscle and the responses of the smooth muscle to nicotinic agonists were studied. (-)-Nicotine was 15 times more effective than (+)-nicotine in releasing ACh. Since tetrodotoxin (1 microM) completely antagonized the effect of nicotinic agonists, the site of action of the nicotinic agonists studied was on the somatodendritic nicotinic receptors. The electrical field stimulation-evoked release was not affected by nicotinic agonists and antagonists, indicating that the axon terminals of cholinergic interneurons are not equipped with nicotinic receptors. This preparation proved to be useful to study the effect of nicotinic agonists on somatodendritic receptors, to determine the affinity constants of nicotinic antagonists, and to characterize these receptors. The rank order of antagonists was d-tubocurarine = mecamylamine greater than pipecuronium greater than pancuronium greater than vecuronium greater than hexamethonium; the apparent affinity constants (KD) were 1.15, 1.55, 3.06, 3.98, 13.59 and 32.88 microM, respectively. alpha-Bungarotoxin had no antagonistic activity at all. This finding indicates that nicotine and the endogenous ligand ACh act via a postsynaptic, somatodendritic nicotinic receptor that is pharmacologically similar to those located on the axon terminals of sympathetic neurons or in ganglions, but is dissimilar to those located at the postsynaptic site of the neuromuscular junction.

Acetylcholine↗
PubMed1999

Nerve terminal nicotinic cholinergic receptors on excitatory motoneurons in the myenteric plexus of guinea pig intestine.

Nicotinic acetylcholine receptors (nAChRs) localized to excitatory longitudinal muscle motoneurons were studied in segments of guinea pig ileum maintained in vitro. Longitudinal muscle contractions caused by the nAChRs agonists, dimethylphenylpiperazinium (DMPP), nicotine, and cytisine were measured using isometric strain gauge transducers. In normal Krebs' solution, the nAChR agonists caused concentration-dependent biphasic contractions with a rank order potency of DMPP > cytisine = nicotine. Contractions caused by DMPP and nicotine were inhibited more than 80% by tetrodotoxin (TTX, 0.3 microM). Responses caused by DMPP were inhibited in a concentration-dependent manner by the competitive nAChR antagonist dihydro-beta-erythroidine (pA(2) = 5.4). In the presence of scopolamine (1 microM) to block muscarinic cholinergic receptors, the nAChR agonists caused longitudinal muscle contractions that were monophasic and smaller in amplitude than those recorded in the absence of scopolamine. With scopolamine present, the agonist rank order potency was nicotine = DMPP > cytisine. Contractions caused by DMPP and nicotine (each at 100 microM) were reduced by TTX by only 52 +/- 7 and 59 +/- 6%, respectively. Noncholinergic contractions caused by DMPP and nicotine were blocked by the neurokinin-1 receptor antagonist, CP 96,345-1 (0.3 microM). Dihydro-beta-erythroidine also inhibited noncholinergic contractions caused by DMPP with a pA(2) value of 5.4. It is concluded that nAChRs are localized to the somatodendritic region of excitatory longitudinal muscle motoneurons. There are also nAChRs localized to the nerve terminals of these neurons where agonists can cause noncholinergic contractions via a TTX-insensitive mechanism.

Animals↗
PubMed2000

Inputs from intrinsic primary afferent neurons to nitric oxide synthase-immunoreactive neurons in the myenteric plexus of guinea pig ileum.

Nitric oxide synthase (NOS) immunoreactivity occurs in two groups of neurons in the guinea pig small intestine: descending interneurons that are also immunoreactive for choline acetyltransferase (ChAT), and inhibitory motor neurons that lack ChAT immunoreactivity. Interneurons that are involved in local reflexes would be expected to have inputs from intrinsic primary afferent (sensory) neurons, most of which are calbindin-immunoreactive. We examined this possibility using triple staining for NOS, ChAT and calbindin immunoreactivity and investigated the relationships between calbindin-immunoreactive varicosities and the cell bodies of NOS-immunoreactive neurons, using high-resolution confocal microscopy and electron microscopy. By confocal microscopy, we found that the cell bodies of ChAT/NOS interneurons received 84 +/- 23 (mean +/- SD) direct appositions from calbindin-immunoreactive varicosities and that the cell bodies of NOS-inhibitory motor neurons received 82 +/- 20 appositions. Electron-microscopic examination of the relations of 265-calbindin-immunoreactive varicosities, at distances within the resolution of the confocal microscope (300 nm), to 30 NOS-immunoreactive nerve cells indicated that 84% formed close contacts or synapses and 16% were separated from neurons by thin glial cell processes. Thus, each NOS-immunoreactive nerve cell receives about 70 synaptic inputs or close contacts from the calbindin-immunoreactive varicosities of intrinsic primary afferent neurons. It is concluded that there are monosynaptic reflex connections in which intrinsic primary afferent neurons synapse directly with motor neurons and di- or poly-synaptic reflexes in which ChAT- and NOS-immunoreactive neurons are interneurons, interposed between intrinsic primary afferent neurons and NOS-inhibitory neurons.

Afferent Pathways↗
PubMed1986

Effect of cholera toxin and pertussis toxin on opioid tolerance and dependence in the guinea-pig myenteric plexus.

Opioid tolerance and dependence are characterized in terms of inhibitory and excitatory neuronal mechanisms. Bacterial toxins were used to investigate these phenomena in the isolated guinea-pig ileum (GPI) and mouse vas deferens (MVD). Cholera toxin (CT) and pertussis toxin (islet activating protein; IAP) have been demonstrated to selectively impair the function of either the stimulatory or inhibitory nucleotide regulatory protein, mediating the signal transmission to the adenylate cyclase. It has been found that CT failed to affect electrically evoked twitch tension in naive and tolerant GPI and MVD. Twitch tension evoked by excitatory drugs, e.g. neurotensin, was attenuated in the GPI, but not in the MVD. CT did not interfere with the actions of opioids or nonopioids in either the GPI or the MVD. Similarly, IAP failed to affect electrically evoked twitch tension. It virtually lacked an effect on the inhibitory action of opioids and nonopioids on electrically stimulated naive and tolerant GPI and MVD. On the other hand, both CT and IAP dose-dependently attenuated the naloxone precipitated withdrawal contracture in the GPI rendered opioid-dependent. These findings may suggest that opioid receptors at nerve terminals of the GPI and the MVD are not linked to adenylate cyclase, and those receptors relate to the state of tolerance. In contrast, opioid receptors located at nerve somata may be linked to adenylate cyclase. Those receptors may be associated with the development of dependence. The experiments with CT suggest a synaptic excitatory input of neighboring nerve elements necessary for the generation of a withdrawal contracture.

Adenylate Cyclase Toxin↗
PubMed1988

Neurokinin3-receptors are linked to inositol phospholipid hydrolysis in the guinea-pig ileum longitudinal muscle-myenteric plexus preparation.

1. Tachykinin-stimulated inositol phospholipid hydrolysis was examined in slices of longitudinal muscle from guinea-pig ileum. 2. Substance P, neurokinin A and neurokinin B induced a concentration-dependent accumulation of total [3H]-inositol phosphates in the presence of 12 mM lithium with similar maximal responses and EC50 values. 3. The selective NK1-receptor agonist, substance P methyl ester, and the selective NK3-receptor agonist succ-[Asp6, MePhe8]-SP(6-11) (senktide) also stimulated [3H]-inositol phosphate formation with maximum responses of 50.69 +/- 0.96 and 45.64 +/- 1.17% relative to 10 microM substance P, respectively. Substance P methyl ester was approximately equipotent with substance P, whereas senktide was approximately 100 times more potent. 4. When added together, maximally effective concentrations of substance P methyl ester and senktide gave responses that were fully additive. In contrast, responses to substance P and neurokinin B were not additive. 5. The stimulation of [3H]-inositol phosphate formation by substance P, neurokinin B and senktide was not affected by atropine (2 microM) or tetrodotoxin (TTX, 0.3 microM). 6. The contractile effect of senktide was inhibited completely by TTX and partially blocked by atropine. Contractions induced by substance P methyl ester were not changed in the presence of TTX or atropine. 7. [D-Pro4, D-Trp7,9,10]-SP(4-11) competitively antagonized the action of substance P methyl ester on inositol phospholipid hydrolysis and contraction, but had no significant effect on senktide-induced inositol phospholipid breakdown or contraction. 8. These results suggest that NK3-receptors in the guinea-pig ileum are coupled to inositol phospholipid hydrolysis.

Animals↗
PubMed2006

Phosphorylation of NMDA NR1 subunits in the myenteric plexus during TNBS induced colitis.

N-Methyl-d-aspartic acid (NMDA) receptors are known to function in the mediation of pain and have a significant role in the development of hyperalgesia following inflammation. Serine phosphorylation regulation of NMDA receptor function occurs in a variety of conditions. No studies have demonstrated a change in phosphorylation of enteric NMDA receptors following colonic inflammation. We examined the levels of NMDA NR1 phosphorylation in trinitrobenzene sulfonic acid (TNBS) induced colitis in rats and compared it to protein translation and the development of visceral hypersensitivity. We have previously, demonstrated an increase in the C1 cassette of NR1 mRNA expression at 14, 21, and 28 days following TNBS administration. In this study, we examined the NR1 serine phosphorylation at 14 days following TNBS injection. Male Sprague-Dawley rats (200-250 g) were treated with TNBS (20mg per rat) diluted in 50% ethanol (n=3) and vehicle controls of 50% ethanol (n=3). TNBS and vehicle controls were administered with a 24 gauge catheter inserted into the lumen of the rat colon. The animals were sacrificed at 14 days after induction of the colitis and their distal colon was retrieved for two-dimensional (2D) western blot analysis. Serine phosphorylation of the NR1 subunit with C1 cassette appears at 14 days after TNBS injection. In contrast, there was no NR1-C1 expression in the vehicle controls and untreated normal controls. These results suggest a role for colonic-NMDA receptor phosphorylation in the development of neuronal plasticity following colonic inflammation. Phosphorylation of NR1 may partially explain visceral hypersensitivity present during colonic inflammation.

Alkaline Phosphatase↗
PubMed1981

Myenteric plexus of the hind-gut: developmental abnormalities in humans and experimental studies.

Intraluminal pressure studies on patients with congenital aganglionosis showed that the aganglionic rectum contracted in an uncoordinated manner and failed to relax. Histochemical assessment of the innervation helped to explain the variable severity of the symptoms in this condition. It is concluded that (1) absence of ganglia prevents normal coordinated peristalsis and creates an obstructive element; (2) absence of reflex relaxation adds to the obstruction; (3) the degree of uncoordinated motor activity in distal aganglionic bowel probably relates to the number of cholinesterase-positive nerves in the circular muscle and adds another variable obstructive element; and (4) deficient innervation of distal ganglionic bowel probably creates a poor propulsive force and so accentuates more distal obstructive factors. Neurohistochemical and functional studies in the anorectum of cats reveal a somewhat different innervation pattern from that in humans but show that sphincteric tone is mainly due to alpha-adrenergic neural activity. Reflex relaxation of the internal anal sphincter is a complex function in which inhibitory responses override motor responses, and it involves an important non-adrenergic non-cholinergic component. The role of cholinergic nerves in the sphincter remains uncertain. Neurohistochemical assessment of full thickness biopsy specimens of rectal muscle from patients with disabling constipation shows that developmental neuronal dysplasias of the hind-gut may be divided into three main categories: (1) aganglionosis (Hirschsprung's disease), (2) hypoganglionosis and (3) hyperganglionosis, and that the different neuronal elements may be affected to differing degrees in individuals within each group. Resection of the aganglionic bowel is required in congenital aganglionosis but the combined diagnostic-therapeutic procedure of anorectal myotomy has been found beneficial in patients with hypoganglionosis.

Animals↗
PubMed1985

Colocalization of dynorphin-A(1-17) and dynorphin-A(1-8) within some perikarya of rat duodenum: immunohistochemical evidence for the presence of two separate dynorphinergic systems.

Adjacent serial sections through the rat duodenum were alternately stained for immunofluorescence microscopic studies with specific anti-sera directed to the opioid peptides dynorphin-A(1-17) and dynorphin-A(1-8), respectively. This resulted in the evidence that two separate dynorphinergic neuron populations are present there: intramural neurons, revealing a colocalization of dynorphin-A(1-17) and dynorphin-A(1-8), were round, contained a large and round nucleus and were lying sporadically in the longitudinal muscle layer as well as bulb-shaped neurons expressing only a dynorphin-A(1-8) immunoreactivity. The latter were recognized abundantly in the myenteric plexus. Myenteric plexus nerve fibres and terminals were immunoreactive for dynorphin-A(1-8), but not for dynorphin-A(1-17). Dynorphin-A(1-8) immunostained nerve terminals formed close contacts with large non-dynorphinergic myenteric plexus perikarya. These findings might indicate that dynorphin-A(1-8) is processed directly from its prodynorphin ('preproenkephalin B') precursor within myenteric plexus perikarya and indirectly via dynorphin-A(1-17) within intramural perikarya, indicating the presence of two separate dynorphinergic systems in the rat duodenum.

Animals↗
PubMed1991

Interaction of trimebutine and Jo-1196 (fedotozine) with opioid receptors in the canine ileum.

Receptor binding of the opioid receptor antagonist, [3H]diprenorphine, which has a similar affinity to the various opioid receptor subtypes, was characterized in subcellular fractions derived from either longitudinal or circular smooth muscle of the canine small intestine with their plexuses (myenteric plexus and deep muscular plexus, respectively) attached. The distribution of opioid binding activity showed a good correlation in the different fractions with the binding of the neuronal marker [3H]saxitoxin but no correlation to the smooth muscle plasma membrane marker 5'-nucleotidase. The saturation data (Kd = 0.12 +/- 0.04 nM and maximum binding = 400 +/- 20 fmol/mg) and the data from kinetic experiments (Kd = 0.08 nmol) in the myenteric plexus were in good agreement with results obtained previously from the circular muscle/deep muscular plexus preparation. Competition experiments using selective drugs for mu [morphiceptin-analog (N-MePhe3-D-Pro4)-morphiceptin] ), delta (D-Pen2,5-enkephalin) and kappa (dynorphin 1-13, U50488-H) ligands showed the existence of all three receptor subtypes. The existence of kappa receptors was confirmed in saturation experiments using [3H] ethylketocycloazocine as labeled ligand. Two putative opioid agonists, with effects on gastrointestinal motility, trimebutine and JO-1196 (fedotozin), were also examined. Trimebutine (Ki = 0.18 microM), Des-Met-trimebutine (Ki = 0.72 microM) and Jo-1196 (Ki = 0.19 microM) displaced specific opiate binding. The relative affinity for the opioid receptor subtypes was mu = 0.44, delta = 0.30 and kappa = 0.26 for trimebutine and mu = 0.25, delta = 0.22 and kappa = 0.52 for Jo-1196. Thus, Jo-1196 had some selectivity for kappa receptors compared to trimebutine. We conclude that there are similar types of opioid receptors in the myenteric plexus and the deep muscular plexus and that specificity of function of opioid nerves must depend on differential location of receptor types on particular neurons. The action of trimebutine and related drugs could vary depending upon their interactions with various gut opioid receptors having different physiological roles.

5'-Nucleotidase↗
PubMed1998

Neural and non-neural activation of electrogenic secretion by 5-hydroxytryptamine in the rat ileum in vitro.

5-hydroxytryptamine (5-HT) stimulates electrogenic Cl- secretion in rat ileum stripped of its outer smooth musculature and myenteric plexus. The myenteric plexus, however, is a site of 5-HT synthesis in the gut, and the plexus mediates electrogenic ion secretion activated by luminal enterotoxin STa and taurocholate. Thus, we investigated the role of the myenteric plexus in 5-HT-induced electrogenic secretion in vitro by measuring short-circuit current (Isc, microamps) with voltage-clamp apparatus as an index of electrogenic Cl-secretion in rat ileum which was either stripped of the myenteric plexus or was left intact. Serosally added 5-HT stimulated electrogenic Cl- secretion in muscle-stripped and intact ileum in a concentration-dependent manner. Pre-treatment of stripped ileum with atropine (1 micron), hexamethonium (100 microns), tetrodotoxin (1.25 microns) and capsaicin (1 micron) for 15 min did not effect the maximum Isc induced by 5-HT which would implicate a direct action on the enterocyte. In intact ilea, however, tetrodotoxin (TTX) and capsaicin reduced significantly the maximum values of Isc stimulated by 5-HT, and the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) caused a significant decrease in the maximum response to 5-HT. These results suggest that electrogenic secretion induced by 5-HT in rat ileum in vitro occurs partly by activation of a non-neural pathway probably involving a direct interaction with the enterocyte, and partly via a nitrinergic-myenteric secretory reflex activated by sensory afferent fibres. These data highlight the danger of characterising intestinal secretory activity from in vitro experiments by using muscle-stripped tissue only.

Animals↗
PubMed1999

Three-dimensional structures of c-Kit-positive cellular networks in the guinea pig small intestine and colon.

Cryosections and whole-mount preparations of the guinea pig small intestine and colon were single or double immunolabeled using the anti-c-Kit and protein gene product 9.5 antibodies. Immunolabeled specimens were observed under a confocal laser scanning microscope. The main findings of the present study are: (1) the distribution and profiles of three-dimensional structures of c-Kit-positive cellular networks in the small intestine and colon, and (2) the anatomical relations of c-Kit-positive cells to the enteric nerves in the layers. In the small intestine, c-Kit-positive cellular networks were observed at levels of the deep muscular plexus and myenteric plexus. The c-Kit-positive cellular networks ran along or overlay the nerve fibers at the deep muscular plexus, while they showed the reticular structures intermingled with the nerve elements at the myenteric plexus. In the colon, c-Kit-positive cellular networks were observed at levels of the submuscular plexus and myenteric plexus, and were further identified within the circular and longitudinal muscle layers as well as in the subserosal layer. In the circular muscle layer, c-Kit-positive cells surrounded the associated nerve fibers and extended several long processes toward the adjacent c-Kit-positive cells. The c-Kit-positive cellular networks within the longitudinal muscle layer as well as in the subserosal layer were not associated with the nerve fibers. In the layers of the intestinal wall with c-Kit-positive cells, the cellular networks of the interstitial cells were identified in ultrastructure. The characteristic profiles of c-Kit-positive cellular networks provide a morphological basis upon which to investigate the mechanisms regulating intestinal movement.

Animals↗
PubMed1999

Immunohistochemical distribution of c-Kit-positive cells and nitric oxide synthase-positive nerves in the guinea-pig small intestine.

Anatomical relationships between c-Kit-positive cells and nitric oxide synthase-positive nerves in the small intestine were examined by double-labeling immunohistochemistry. Cryosections and whole mount preparations of the guinea-pig small intestine were double-immunolabeled using anti-c-Kit and neuronal nitric oxide synthase antibodies, and were observed using confocal laser scanning microscopy. The c-Kit-like immunoreactivity constituted dense reticular networks in the deep muscular plexus and myenteric plexus of the intestinal wall. The nitric oxide synthase-like immunoreactivity occurred in the circular muscle layer, most densely at the deep muscular plexus, as well as within the ganglion strands or connecting strands of the myenteric plexus. Close association between c-Kit-like immunoreactivity and nitric oxide synthase-like immunoreactivity was evident in the deep muscular plexus. Specimens immunolabeled with the anti-nitric oxide synthase antibody were further examined under transmission electron microscopy. Axon profiles with nitric oxide synthase-like immunoreactivity lay closely adjacent to the interstitial cells in the deep muscular plexus as well as to smooth muscle cells of the circular muscle layer, whereas there was a considerable distance (> 500 nm) between interstitial cells and axon profiles with nitric oxide synthase-like immunoreactivity in the myenteric plexus. These results suggest that the interstitial cells in the deep muscular plexus serve as mediators of the nitrergic neurotransmission to the musculature in the small intestine, playing a role in the regulation of intestinal movement.

Animals↗