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PubMed1985

A simultaneous demonstration of particular enteric neuronal cell types with the NADH:nitro BT-dehydrogenase reaction and of nerve fibres containing enkephalin-like immunoreactivity in the myenteric plexus of the porcine small intestine.

The myenteric plexus of the porcine small intestine is studied using a combined method for the simultaneous visualization of enteric intramural neuronal cell bodies and peptidergic nerve fibers. As earlier reported, the histochemical method for demonstration of the NADH-dependent dehydrogenase reaction allows the identification of the three neuron types of Dogiel but, in addition, the afore mentioned staining method creates fair conditions in the tissue for the subsequent indirect immunocytochemical visualization of neuropeptides, as demonstrated in this work by means of the indirect immunofluorescence method for enkephalin-like immunoreactivity. Intense fluorescent varicosities of enkephalin-like nerve fibres were found to ramify around dark-blue stained ganglionic cells of type I, type II and type III in a manner suggestive of innervation.

Animals↗

PubMed1989

Chronic opiate receptor activation in vivo alters the level of G-protein subunits in guinea-pig myenteric plexus.

Studies with the longitudinal muscle-myenteric plexus preparation of the guinea-pig ileum were undertaken to investigate the relationship between guanine nucleotide-binding proteins (G-proteins) and chronic opioid receptor activation in vivo. Treatment with the narcotic agonist fentanyl, at doses which render the preparation tolerant and dependent, led to an increase of pertussis toxin-catalysed incorporation of ADP-ribose in a protein of approximately 40,000 mol. wt. Quantitative immunoblotting, using site-directed antisera, demonstrated an upregulation of G alpha i/G alpha o and, to an even greater degree, of G beta. However, the level of G alpha s was decreased by the same treatment. All alterations observed were abolished by the concomitant presence of the antagonist naloxone. The implications of this differential regulation of G-protein subunits for opiate-induced tolerance and dependence are discussed.

Adenosine Diphosphate Ribose↗

PubMed1991

Involvement of mu, delta and kappa receptors in morphine-induced tolerance in the guinea pig myenteric plexus.

Tolerance in the longitudinal muscle-myenteric plexus (LM-MP) preparation to opioids appears to represent two separate phenomena. One phenomenon is characterized by marked subsensitivity to mu-selective opioid substances and a very short half-life. The other is characterized by moderate subsensitivity to morphine and to several nonopioid inhibitory substances and has a long half-life. The present investigation was to determine if the long half-life type of tolerance involves cross-tolerance between mu-selective opioids, such as morphine, and opioids selective for delta or kappa receptors. Tolerance was induced by s.c. implantation of morphine pellets for 7 days. Control guinea pigs received placebo pellets. Isolated LM-MP preparations were tolerant to the mu-selective agonists morphine and [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin as well as to [D-Ala,2D-Leu5]enkephalin and [D-Ser2]leucine enkephalin-Thr, agonists only slightly selective for delta receptors over mu. The delta-selective agonist, [D-Pen2,D-Pen3]enkephalin, produced a biphasic concentration-response curve. The first phase, which included only very weak effects, presumably represented delta-mediated effects. The second phase reached virtually 100% inhibition of the twitch. Significant subsensitivity (tolerance) was demonstrated only for the second phase, presumably representing mu-mediated effects. There was no significant tolerance to the kappa-selective agonist, U50,488H. Consistent with the literature, the results indicate effective twitch inhibition mediated by mu and kappa receptors, but not delta receptors. Among opioids, tolerance induced by morphine pellets in the LM-MP is limited to mu receptor-mediated inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Effects of GABA in the morphine-tolerant longitudinal muscle, myenteric plexus preparation of the guinea pig.

The effect of chronic treatment with morphine via pellet implantation on the sensitivity of the longitudinal smooth muscle-myenteric plexus of the guinea pig ileum to the contractile effects of gamma-aminobutyric acid (GABAA)-receptor agonists was assessed. GABA and muscimol elicited concentration-dependent contractions of the longitudinal smooth muscle which were due to the release of acetylcholine because the contractile effects were markedly attenuated by atropine (10 nM). The contractile action of GABA agonists does not involve an intermediate step mediated by nicotinic receptors because the concentration-response curves for GABA were unaffected by hexamethonium (1 mM). Bicuculline (10 microM) produced nearly equivalent rightward shifts of the concentration-response curves for both GABA and muscimol, indicating mediation of the contractile effects of these agents by GABAA receptors. Chronic exposure to morphine via pellet implantation did not alter the sensitivity of this preparation to either GABA or muscimol. This is in contrast to the development of supersensitivity of the longitudinal smooth muscle-myenteric plexus to other excitatory agonists (nicotine, 5-hydroxytryptamine and potassium), which accompanies the development of tolerance to opioids. GABA induces depolarization of myenteric neurons that is observed most prominently in AH neurons and rarely in S neurons. The stimulatory effects of nicotine and of GABA were inhibited by morphine (a predominantly mu opioid agonist) and by U50,488H (a predominantly kappa opioid agonist). The results are discussed within the context that supersensitivity to neuronal stimulants of the myenteric plexus in morphine-tolerant preparations is limited to substances which depolarize S neurons.

Animals↗

PubMed1984

[Sensitivity of neurons of the myenteric plexus to opiate alkaloid morphine].

With the aid of sucrose gap method, sensitivity of the myenteric plexus' neurons was studied in the neural-muscular preparation which included the myenteric plexus and circular smooth muscle layer. Morphine (10(-4)-10(-8) g/ml) produced an excitation as revealed in depolarization of the smooth muscle cell membrane, in the increase of AP frequency and amplitude as well as of the duration of contractions. Incubation of the preparation in the solution containing M- and N-cholinergic blocking drugs (10(-5) g/ml atropine and 5 X 10(-6) g/ml benzohexonium) and preadministration of the antagonist of opiate receptors naloxone (3 X 10(-7) g/ml) did not change the character of morphine action, whereas administration of serotonin antagonist methysergide (5 X 10(-6) g/ml) eliminated the excitatory effects. These changes in electrical and contractile activity of the preparation after morphine administration seem to be connected with an increasing release of serotonin.

Action Potentials↗

PubMed2002

Tea catechin, (-)-epigallocatechin gallate, facilitates cholinergic ganglion transmission in the myenteric plexus of the guinea-pig small intestine.

Intracellular recordings were made from myenteric S neurons of the guinea-pig ileum. One of the major tea catechins, (-)-epigallocatechin gallate (EGCG at concentrations from 1 to 20 microM), was applied by superfusion to examine its effect on cholinergic ganglion transmission in the myenteric plexus. Fast excitatory postsynaptic potentials (EPSPs) evoked by electrical stimulation to ganglia and/or internodal fiber tracts were augmented in amplitude by EGCG in about 60% of tested neurons without changing the postsynaptic sensitivity to acetylcholine (ACh) applied by ionophoresis. Furthermore, the amplitude-ratio of paired fast EPSPs was increased by EGCG. These results indicated that the site at which EGCG augmented the fast EPSPs was presynaptic. It is concluded that EGCG can facilitate the cholinergic ganglion transmission possibly by increasing the amount of ACh released and, together with its previously described depolarizing action on myenteric neurons, may modulate the activity of the myenteric plexus of the guinea-pig ileum.

Acetylcholine↗

PubMed1998

Projections of submucous neurons to the myenteric plexus in the guinea pig small intestine.

The distribution of submucous neurons that project to the myenteric plexus of the guinea pig small intestine was established by retrograde transport of the carbocyanine dye 1,1'-didodecyl-3,3,3',3'-tetramethyl indocarbocyanine perchlorate (DiI) from myenteric ganglia in organ culture in combination with immunohistochemistry. Following the application of DiI to the serosal surface of a single myenteric ganglion, from 2 to 15 DiI-labelled nerve cell bodies were labelled in the submucous plexus up to 7.9 mm circumferentially, 4.5 mm orally, and 3.4 mm aborally to the DiI application site. No cells were labelled in preparations in which connections between myenteric and submucous plexuses had been severed prior to DiI application. Cells that were immunoreactive for vasoactive intestinal polypeptide (VIP) or for substance P (SP) accounted for about 75% and 11% of DiI-labelled cells, respectively. Neither neuropeptide Y- nor calretinin-immunoreactive submucous neurons were labelled by DiI, indicating that these classes of neurons do not project to the myenteric plexus. Retrograde tracing from the myenteric plexus with Neurobiotin revealed that labelled VIP-immunoreactive neurons had several short, filamentous processes and a single long axon that could be followed through the circular muscle to myenteric ganglia without branches to the mucosa. The previously described projection of submucous, SP-immunoreactive putative sensory neurons to the myenteric plexus was confirmed. However, this study has identified a considerably larger population of presumed interneurons that are immunoreactive for VIP that likely transmit information from the submucous plexus to the myenteric plexus and presumably coordinate activity between the two ganglionated plexuses.

Animals↗

PubMed1983

Postnatal development of the myenteric plexus in cat stomach.

The postnatal development of the myenteric plexus in cat stomach has been studied at birth, on the 14th, 30th, 45th and 180th postnatal days, using light- and electronmicroscopic methods. In newborn kittens the main network of the Auerbach plexus is well formed, but the myenteric ganglia are composed of nerve cells with different maturity and a scarce neuropile. During the first two postnatal weeks the dimensions of the ganglia increase owing to the increase of the nerve bodies and the rising number of glials cells and intercellular fibres. This is accompanied by a potentiation of the AChE-activity, mainly in the nerve cell bodies and to a lesser extent in the neuropile. Impregnation reveals different in calibre and form nerve fibres and terminals. Different ultrastructural types of neurones are identified on the 14th day. Later development is expressed in the formation of large compact ganglia and thick connecting strands. The number of AChE-positive fibres in the neuropile increases. Owing to the increase in the cell organelles and their more advanced maturity, it is possible to define the ultrastructural type of an ever increasing number of neurones.

Acetylcholinesterase↗

PubMed1992

Nicotinic receptor-evoked release of acetylcholine and somatostatin in the myenteric plexus is coupled to calcium influx via N-type calcium channels.

Entry of extracellular calcium (Ca++) via voltage-gated Ca++ channels is essential for neurotransmitter release. In this study, we examined whether nicotinic receptor-stimulated release of acetylcholine (ACh) and somatostatin (S14) are coupled to calcium influx via distinct calcium channel subtypes in the myenteric plexus. Isolated ganglia from the guinea pig ileal myenteric plexus were prepared and placed in perfusion chambers under standard conditions. The ganglionic agonist dimethylphenylpiperazinium (DMPP, 10(-6) to 10(-3) M) stimulated the release of [3H]ACh in a concentration-dependent manner. This release was blocked by hexamethonium or Ca(++)-free medium containing 1 mM EGTA and was antagonized by omega-conotoxin, a preferential N calcium channel blocker, but was not affected by nifedipine (L channel antagonist) or nickel (T calcium channel antagonist). DMPP-evoked release of somatostatin was also antagonized by omega-conotoxin, but was not affected by nifedipine or nickel. These observations indicate that neurosecretion of ACh and S14 evoked by DMPP is mediated by calcium entry via voltage-sensitive N-type Ca++ channels. To provide additional evidence that nicotinic receptor stimulation is associated with Ca++ entry via the N-type Ca++ channels, we examined the intracellular calcium [Ca++]i concentration of the myenteric plexus neurons using fura-2 microspectrofluorometry. Basal [Ca++]i of single ileal myenteric neurons was 65 +/- 5 nM. Perfusion with DMPP (10(-6) to 10(-3) M) caused a rapid, transient elevation in [Ca++]i which was abolished by Ca(++)-free medium containing 1 mM EGTA.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1988

The forms of argyrophilic ganglion cells in the myenteric plexus throughout the gastrointestinal tract of the opossum.

In the small intestine, the myenteric plexus contains several different forms of ganglion cells. We examined the whole gut of the American opossum to see if these forms exist in other organs. Sections were stained by silver-impregnation. About half the ganglion cells were argyrophilic in all regions. Argyrophilic cells were described as to dendrite shape (filiform or lamellar), number, and grouping on the nerve cell body (radiating or focal), and in respect to nuclear position (central or peripheral). Cells with lamellar dendrites were sparse in esophagus (less than 5%), in gastric fundus (17.2%) and in antrum (8.2%), increased from duodenum (18.5%) to ileum (64.3%) and increased along the colon from the cecum (62.3%) to the rectum (94.9%). The proportion of cells with filiform dendrites diminished correspondingly along the gut. The number of dendrites per cell increased caudad along the gut. Cells with focally distributed dendrites were rare in all regions. More cells had central nuclei than peripheral nuclei in all regions, and nuclear position did not correlate with dendrite morphology. Thus, the forms of myenteric plexus ganglion cells differ systematically in the gut. The results do not support the idea that a specific function can be assigned to a ganglion cell of a specific form.

Animals↗

PubMed1998

Relationship between inhibitory effect of endogenous opioid via mu-receptors and muscarinic autoinhibition in acetylcholine release from myenteric plexus of guinea pig ileum.

Relationship between activation of opioid receptors and muscarinic autoinhibition in acetylcholine (ACh) release from the myenteric plexus was studied in longitudinal muscle myenteric plexus (LMMP) preparations of guinea pig ileum. A mu-receptor agonist, [D-Ala2, N-Me-Phe4, Gly5-ol] enkephalin (DAMGO), at a concentration of 1 microM inhibited the ACh release evoked by electrical field stimulation (EFS) at 1 Hz but not at 10 Hz. After the muscarinic autoreceptors were blocked with atropine (1 microM), DAMGO inhibited EFS-evoked ACh release also at 10 Hz. After the autoreceptors were potently activated with muscarine (200 microM), the inhibitory effect of DAMGO at 1 Hz was abolished. A kappa-receptor agonist, U-50,488, at 1 microM inhibited the EFS-evoked ACh release both at 1 and 10 Hz. U-50,488 inhibited ACh release regardless of the presence of atropine or muscarine. A delta-agonist, enkephalin [D-PEN2.5] (PDPDE), did not show any significant effect. On the other hand, a selective mu-receptor antagonist, cyprodime, increased ACh release evoked by EFS at 1 Hz, but not at 10 Hz. After the autoreceptors were blocked, cyprodime increased EFS-evoked ACh release also at 10 Hz. The selective kappa-receptor antagonist, nor-binaltorphimine, did not affect ACh release in the absence or presence of atropine. The results suggest that endogenous opioid(s) inhibits ACh release by activating mu-, but not kappa- and delta-receptors in the LMMP of guinea pig ileum and that the inhibitory effect of endogenous opioid(s) in the ACh release is important when muscarinic autoinhibition mechanism does not fully work.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1976

Esophageal aperistalsis secondary to metastatic invasion of the myenteric plexus.

A case of aperistalsis of the esophagus secondary to isolated invasion of the myenteric plexus of Auerbach by metastatic carcinoma is presented. The unique pattern of tumor involvement and the resultant aperistalsis supports the contention that involvement of the neurons in the deep myenteric plexus, either by inflammation or tumor, may be the key factor in producing aperistalsis. No similar cases were found in the literature.

Aged↗

PubMed1990

An immunohistochemical study of the myenteric plexus of the colon in the rat and mouse.

Immunohistochemical methods were used to determine the localisation of immunoreactivities to a variety of antigens involved in neurotransmission in the myenteric plexus of the colon in the rat and mouse. The findings in the two species were closely similar. Five neuronal types have been identified. (i) The axons of extrinsic noradrenergic sympathetic neurons, immunoreactive for tyrosine hydroxylase, supply the ganglia and the circular muscle. (ii) Bombesin immunoreactive intrinsic neurons with unbeaded axons are largely confined to the ganglia and tracts of the plexus. These neurons probably contain gastrin-releasing peptide, which is the mammalian analogue of bombesin. (iii) Somatostatin immunoreactive intrinsic neurons have long, beaded axons within the myenteric plexus and also outside the plexus, between the longitudinal and circular muscle layers. (iv) Intrinsic neurons containing opioid peptides (beta-endorphin, met-enkephalin, leu-enkephalin), have beaded axons that cannot be traced for long distances. They contact all the cell bodies in the ganglia and extend also into the interganglionic tracts and the smooth muscle. (v) Substance P immunoreactive somata and axons are present throughout the myenteric plexus and provide dense innervation to the smooth muscle. Extrinsic substance P immunoreactive sensory axons are probably also present.

Animals↗

PubMed1984

Excitatory synaptic potentials due to activation of neurons with short projections in the myenteric plexus.

Intracellular microelectrodes have been used to examine the effects, on excitatory inputs to myenteric nerve cells, of lesions of intrinsic pathways in the myenteric plexus of the guinea-pig small intestine. The lesions consisted of circumferential cuts (myotomies) which severed the external musculature to the depth of the submucosa and thus interrupted pathways in the myenteric plexus. Sufficient time was allowed between creating the lesions and recording from the neurons for the endings of severed neurites to degenerate and this was confirmed histochemically by examining the distribution of varicose fibres with 5-hydroxytryptamine immunoreactivity in myenteric ganglia from which recordings were made. Two types of excitatory input, eliciting fast and slow excitatory post-synaptic potentials, respectively, were demonstrable in response to focal stimulation of nerves in the ganglia from which recordings were made. There were no differences in the proportions of neurons in which fast or slow excitatory synaptic potentials were evoked in unoperated preparations (controls), in islands 1.5-4 mm wide between myotomies, or within 1 mm on the oral or anal sides of myotomies. Possible differences in the amplitudes, durations at half amplitude, and threshold numbers of stimuli for initiation of slow excitatory synaptic potentials were analyzed. The only significant differences were found when data from control and oral areas were pooled and compared with combined data from island and anal areas (this assessed differences that could arise from severing nerve fibres running from oral to anal).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2000

Decreased expression of nitric oxide synthase in the colonic myenteric plexus of aged rats.

Nitric oxide (NO) is a major non-adrenergic, non-cholinergic (NANC) inhibitory neurotransmitter in the gastrointestinal tract. NO released from the myenteric plexus enhances colonic transit and facilitates propulsion of the colonic contents by mediating descending relaxation. Although it has been suggested that colonic transit delays with aging, the mechanism of delayed colonic transit in aging remains unclear. We hypothesized that advanced age is associated with decreased expression of neuronal NO synthase (nNOS) and concomitant reduction in synthesis of NO in the rat colon. We studied nNOS mRNA expression, nNOS-immunohistochemistry, nNOS-immunoblotting and NOS catalytic activity in the mid-colon obtained from young (age 4-8 months) and aged (age 22-28 months) Fisher (F344xBN)F1 rats. Western blot analysis of PGP 9.5, a generic neuronal marker, of the colonic tissues were employed to study whether the total number of neurons of the myenteric plexus is reduced with aging. The number of nNOS-immunoreactive cells and nNOS synthesis in the colonic myenteric plexus were significantly reduced in aged rats. In contrast, expression of PGP 9.5 in colonic tissues was not affected in aged rats. Northern blot analysis demonstrated that the expression of neuronal nNOS mRNA was significantly reduced in the colonic tissues in aged rats. Basal and veratridine-induced release of L-[(3)H]citrulline were significantly decreased in colonic tissues from aged rats, compared to young rats. It is suggested that advanced age is associated with diminished gene expression of nNOS, nNOS synthesis and catalytic activity of NOS. This may explain the mechanism of delayed colonic transit observed in advanced age.

Aging↗

PubMed2005

Motilin inhibits ganglionic transmission in the myenteric plexus of the guinea-pig ileum.

Motilin is a key factor in triggering interdigestive migrating contractions. Our preceding study demonstrated that motilin caused membrane depolarizations in a minority of S and AH neurons in the myenteric plexus of the guinea-pig ileum after 18 h-fasting period; motilin depolarizations were small and seldom triggered action potentials. Then, the present study was undertaken to examine possible electrophysiological actions of motilin on the ganglionic transmission in the myenteric plexus. Intracellular recordings with sharp glass microelectrodes were made from myenteric S neurons having fast excitatory postsynaptic potentials (EPSPs), evoked by focal electrical stimulation. Motilin inhibited the fast EPSPs in amplitude, associated either with or without membrane depolarizations. Results obtained with the paired stimulus method suggested that the site for motilin-induced inhibition of fast EPSPs might be presynaptic. Furthermore, motilin did not decrease postsynaptic sensitivity to ACh, a main neurotransmitter mediating the fast EPSPs. Therefore, it is concluded that motilin might inhibit presynaptically ganglionic transmission in the myenteric plexus of the guinea-pig ileum.

Animals↗

PubMed2004

Development of nerves expressing P2X3 receptors in the myenteric plexus of rat stomach.

Development of neurones and fibres expressing P2X3 receptors in the myenteric plexus of rat stomach and coexistence of the P2X3 receptor with calbindin, calretinin and NOS during postnatal development, were investigated with immunostaining methods. Extrinsic nerves expressing P2X3 receptors appeared as early as E12 and were localised in the trunk and branches of the vagus nerve, which extended rapidly onto the whole rat stomach from E12 to E14. Intrinsic neurone cell bodies with P2X3-immunoreactivity in the myenteric ganglia were first demonstrated postnatally at P1, and at P14, when the number of neurones expressing the P2X3 receptor peaked at 45%. P2X3 receptor-immunoreactivity decreased subsequently, and at P60 only about 11% were P2X3-immunoreactive. Intraganglionic laminar nerve endings and intramuscular arrays were first demonstrated postnatally at P1 and P7, respectively. In the early postnatal days, there were many growth cone-like structures with strong P2X3 immunostaining associated with these endings and arrays. Double-immunostaining showed that 9-15% of P2X3-immunoreactive neurones in the gastric myenteric plexus expressed calbindin D-28 k only in the early postnatal days, while 14-21% of neurones from P1 to P60 increasingly expressed calretinin. About 20% of neurones with P2X3 immunoreactivity coexpressed NOS throughout perinatal development.

Animals↗

PubMed1983

Prenatal development of the myenteric plexus in cat stomach.

The prenatal development of the myenteric (Auerbach) plexus in cat stomach has been studied light- and electronmicroscopically. Neuroblasts and axon bundles of the myenteric plexus are found in the gastric wall of the smallest embryos studied (10-15 mm) even before its layers are formed. The plexus elements are not separated from the mesenchyme with a basal membrane. In the larger embryos (40-55 mm) the myenteric plexus is already between two muscle layers. The ganglia are shaped and contain more neuroblasts. A small part of the nerve cells are advanced in their maturation--primary and secondary dendrites are emanated and they are slightly AChE-positive. The maturation of the nerve perikarya is intense during prenatal life. In 95-115 mm long embryos the differentiation of a considerable part of the nerve cells is advanced and it is possible to distinguish some ultrastructural types of myenteric neurones. The number of AChE-positive neuroblasts is increased and there are more dendritic profiles in the neuropile.

Acetylcholinesterase↗