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At least 559 records · Page 31Linked to original sources
PubMed1994

Cross-tolerance between mu- and kappa-opioid agonists in the guinea pig ileum myenteric plexus.

The present investigation was aimed at elucidating if chronic activation of mu opioid receptor induces development of tolerance to mu (specific tolerance) and kappa agonists (cross-tolerance) in the guinea pig ileum myenteric plexus-longitudinal muscle strip. Morphine (prototype of mu agonist), [D-Ala2,N-MePhe4,Gly-ol5]enkephalin (DAMGO) and sufentanil (selective mu-agonists) and U-50,488H (selective kappa agonist) were selected. Tolerance to morphine was induced by subcutaneous implantation of morphine pellets (75 mg per pellet) for 7 days. Tolerance to sufentanil was induced by subcutaneous implantation of osmotic minipumps for 7 days, which deliver at a rate of 2 micrograms/microliters/hr. Control groups received placebo pellets or minipumps of vehicle. Tolerance to morphine and DAMGO was observed after chronic treatment with morphine or sufentanil and was revealed as a rightward shift of the concentration-response curve. In addition, a decrease in maximal response was observed. Preparations from morphine-pelleted guinea pigs were also tolerant to the kappa-selective agonist trans-(+-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidynyl)- cyclohexyl]benzeneacetamide (U-50,488H); that is, there was cross-tolerance to the kappa agonist. The development of tolerance to U-50,488H was characterized by a parallel rightward shift of the concentration-response curve, but the maximal response was unchanged. Sufentanil-tolerant tissues were also tolerant to the inhibitory effects of U-50,488H (cross-tolerance). These data indicate that alterations occur during chronic mu opioid administration that are not receptor specific and suggest that tolerance would be associated with a functional change in the myenteric neurons that is unrelated to individual receptor system.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed2002

Depolarization-evoked GABA release from myenteric plexus is partially coupled to L-, N-, and P/Q-type calcium channels.

1. There are many evidences suggesting that gamma-aminobutyrate (GABA) is an important neurotransmitter and/or neuromodulator in the gut. 2. Using the myenteric plexus-longitudinal muscle preparation from the guinea pig ileum, we investigated the evoked release of [3H] GABA from enteric neurons by electrical pulses or high KCl, which occurs in a calcium-dependent and -independent way. In addition, using selective calcium channel blockers, we report the participation of distinct subtypes of calcium channels in the evoked release, showing a minor participation of L- and Q-type calcium channels, while N- and P-type have a participation of approximately 15%, each. However, regardless of the combination of Ca2+ channel blockers, we did not observe an inhibition greater than 50% of the calcium-dependent component of [3H] GABA release. 3. Thus, while the observed Ca2+-independent release mostly probable occur via reversal of the membrane GABA transporter, in our conditions, a considerable portion of the Ca2+-dependent evoked release of [3H] GABA is not coupled to L-, N-, or P/Q-type calcium channels, suggesting the involvement of intracellular calcium stores or other ways of getting calcium across the membrane.

Action Potentials↗
PubMed1983

Acetylcholine releases ATP from varicosities isolated from guinea pig myenteric plexus.

The effects of cholinergic agonists and antagonists on the release of ATP from isolated myenteric varicosities were studied using a firefly luciferin-luciferase technique. In a previous study, acetylcholine and nicotine released ATP from isolated myenteric varicosities, whereas the muscarinic agonist bethanechol did not. In the present study, release of ATP by acetylcholine was shown to be Ca2+ dependent. d-Tubocurarine competitively antagonized the release of ATP by either acetylcholine or nicotine. Maximal release of ATP by acetylcholine (10(-3) M) was approximately 24% that observed with the depolarizing drug veratridine (5 X 10(-5) M), suggesting either that not all of the varicosities capable of releasing ATP possess nicotinic receptors or that acetylcholine does not depolarize the varicosities to the degree that veratridine does. Tetrodotoxin slightly but significantly reduced ATP release induced by acetylcholine or nicotine, indicating some involvement of Na+ channels in the release process. Finally, 6-hydroxydopamine pretreatment produced a 48% reduction in the acetylcholine-evoked release of ATP, suggesting that much, but possibly not all, of the ATP release occurs from noradrenergic varicosities present in the preparation.

Acetylcholine↗
PubMed1987

Purinergic inhibition in the small intestinal myenteric plexus of the guinea-pig.

1. The actions of adenosine on electrical behaviour of myenteric neurones were investigated with intracellular recording methods in guinea-pig small intestine. 2. The actions of adenosine were: membrane hyperpolarization, decreased input resistance, enhancement of post-spike hyperpolarizing potentials and suppression of excitability. These effects were observed exclusively in AH/type 2 myenteric neurones. 3. The presence of adenosine in the micromolar range of concentrations prevented or suppressed excitatory responses to forskolin. It also aborted the effects of forskolin when added in combination with this activator of adenylate cyclase. 4. Adenosine (100 microM) did not affect the excitatory actions of intracellularly injected cyclic AMP, membrane-permeant analogues of cyclic AMP, inhibitors of cyclic nucleotide phosphodiesterase or elevation of Mg2+ and reduction of Ca2+ in the bathing medium. 5. The results suggest that the mechanism of the inhibitory action of adenosine is suppression of the catalytic activity of adenylate cyclase and consequent reduction of intraneuronal levels of cyclic AMP.

Action Potentials↗
PubMed1993

Functional evidence that [3H]acetylcholine and [3H]noradrenaline release from guinea pig ileal myenteric plexus and noradrenergic terminals is modulated by different presynaptic alpha-2 adrenoceptor subtypes.

The effects of a series of alpha-2 adrenoceptor agonists and antagonists were examined on the stimulation-evoked release of tritium from a myenteric plexus-longitudinal muscle preparation of guinea pig ileum preincubated with [3H]choline or [3H]noradrenaline. Oxymetazoline, xylazine, detomidine and alpha-methylnoradrenaline caused a significant and concentration-dependent inhibition of the stimulation-evoked release of [3H]acetylcholine, with calculated IC50 values of 1.22 microM, 0.88 microM, 0.93 microM and 0.83 microM, respectively. Idazoxan (1 microM), CH 38083 (1 microM), WB 4101 (1 microM), prazosin (1-10 microM) and ARC 239 (1-10 microM) did not significantly affect the evoked release of [3H]acetylcholine. However, idazoxan, CH 38083 and WB 4101 antagonized the inhibitory effect of all agonists tested on [3H]acetylcholine release with calculated KB values in the nanomolar range, whereas prazosin and ARC 239 were ineffective. After incubation of ileum strips with [3H]noradrenaline, the stimulation-evoked release of tritium was significantly inhibited by oxymetazoline (0.1-1000 microM), xylazine (0.1-100 microM), detomidine (0.1-100 microM) or alpha-methyl-noradrenaline (0.1-100 microM), whereas it was enhanced by idazoxan (0.1-100 microM), CH 38083 (0.1-100 microM), WB 4101 (0.1-100 microM), prazosin (0.1 microM) and ARC 239 (0.1-100 microM). The order of potency found for these drugs in affecting the evoked release of [3H]noradrenaline was: xylazine > or = detomidine > alpha-methyl-noradrenaline >> oxymetazoline for agonists and ARC 239 > or = idazoxan > CH 38083 > WB 4101 for antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1999

Immunohistochemical evidence for the presence of calbindin containing neurones in the myenteric plexus of the guinea-pig stomach.

Using immunohistochemistry we studied the presence of calbindin in myenteric neurones of the guinea-pig stomach. A rabbit anti recombinant rat calbindin-D28k (CALB) stained 12, 12 and 25% of all myenteric neurones in the fundus, corpus and antrum, respectively. A rabbit anti recombinant human CALB stained 4, 4 and 16%, respectively. A mouse monoclonal antibody against the chicken intestinal CALB showed no labelling. In all regions most calbindin neurones were additionally choline acetyltransferase (ChAT) positive while only a small proportion exhibited nicotinamide adenosine dinucleatide phosphate (NADPH)-diaphorase-activity. Numerous calbindin-positive varicose nerve fibres were present within myenteric ganglia, rarely detectable in the muscle layers and virtually absent in the mucosa. This study demonstrated that a supopulation of cholinergic myenteric neurones in the stomach contain calbindin and suggested that many of these neurones fulfil interneuronal tasks.

Animals↗
PubMed1984

Actions of gamma-aminobutyric acid on neurones of guinea-pig myenteric plexus.

The effects of gamma-aminobutyric acid (GABA) applied by ionophoresis, pressure ejection and superfusion to myenteric neurones of the guinea-pig ileum were investigated by intracellular recording techniques. Ionophoretic or pressure application of GABA (10 pC-30 nC) caused membrane depolarizations of AH neurones but not S neurones. This depolarization was associated with a conductance increase. It reversed polarity at a membrane potential of -18 mV when intracellular electrodes contained KCl, and -39 mV when electrodes contained K acetate, citrate or sulphate. The ionophoretic depolarization was antagonized by bicuculline (1-30 microM) in an apparently competitive manner. During prolonged or repeated ionophoretic application of GABA, both the depolarization and conductance increase desensitized. Superfusion of GABA (1-100 microM) caused a membrane depolarization in AH neurones, associated with an increase in membrane conductance. The increase in conductance was always smaller than that evoked by ionophoresis of GABA. Bicuculline only partially depressed the depolarization induced by superfusion of GABA, particularly slowing its rising phase. beta-p-Chlorophenyl GABA (baclofen) (10 microM) caused a depolarization similar to that observed with GABA in the presence of bicuculline. The depolarization induced by baclofen and GABA (in presence of bicuculline) superfusion did not decline during prolonged applications; superfusion of GABA but not baclofen reversibly reduced or eliminated the effects of GABA ionophoresis. It is concluded that GABA has two effects on the membrane of myenteric neurones. The first is a bicuculline-sensitive, rapidly desensitizing chloride activation: the second is a bicuculline-insensitive, non-desensitizing depolarization.

Acetylcholine↗
PubMed1984

Inhibition of calcium spikes and transmitter release by gamma-aminobutyric acid in the guinea-pig myenteric plexus.

The effect of gamma-aminobutyric acid (GABA) (1 microM-1 mM) on synaptic transmission in isolated myenteric ganglia of guinea-pig ileum was investigated with intracellular recording techniques. GABA (up to 1 mM) had no effect on the resting membrane potential and membrane conductance of S neurones. GABA reduced the amplitude of the fast excitatory postsynaptic potential e.p.s.p.) without changing the amplitude of the nicotinic response to ionophoretic application of acetylcholine (ACh). This effect was mimicked by baclofen (10-100 microM) and was not blocked by bicuculline (10 microM). The preparation did not become desensitized during prolonged GABA applications. Cholinergic and non-cholinergic slow e.p.s.ps evoked by single or repetitive presynaptic nerve stimulation were reduced in amplitude by GABA. GABA did not depress muscarinic responses to ionophoretic application of ACh. GABA reduced the duration of the action potential in AH neurones in concentrations that did not affect the membrane potential or conductance. The effect was very marked when electrodes were filled with CsCl, and tetrodotoxin was in the superfusing solution. This effect was also mimicked by baclofen, was insensitive to bicuculline and was not reduced with repeated application or GABA. It is concluded that GABA inhibits release of ACh and the transmitter mediating the slow e.p.s.p. This effect may result from inhibition of an inward calcium current.

Action Potentials↗
PubMed1998

Cocaine- and amphetamine-regulated transcript (CART) peptide immunoreactivity in myenteric plexus neurons of the rat ileum and co-localization with choline acetyltransferase.

Cocaine and amphetamine regulated transcript (CART) encodes a novel brain-enriched protein whose features are reminiscent of a neurotransmitter propeptide. We have now localized CART peptide(s) in the gastrointestinal tract by immunohistochemical methods. Polyclonal antisera raised to CART peptide 106-129 stained neuronal cell bodies and fibers in rat ileum myenteric plexus-longitudinal muscle tissue preparations. Electron microscopic analysis of thin sections showed immunopositive axon terminals in close apposition to CART-labelled and unlabelled neuronal cell bodies as well as to the longitudinal muscle. CART peptide-immunoreactive terminals contained numerous ovoid electron-lucent vesicles and a few dark-stained dense-core vesicles. Light microscopic double labelling studies revealed CART peptide immunoreactivity in a subpopulation of choline acetyltransferase (ChAT)-immunoreactive neurons. This combined light microscopic and ultrastructural examination of CART peptides in the gastrointestinal tract suggests a role of CART peptides as transmitters or neuromodulators in the peripheral nervous system.

Animals↗
PubMed1983

Ontogenesis of the myenteric plexus in the cat gastro-intestinal sphincters. II. Axonal differentiation.

The differentiation of the axons in the cat myenteric ganglia of the gastro-intestinal sphincters has been examined during pre- and postnatal development. The quantitative analysis has been also used. The differentiation of the axons was a prolonged process that advanced parallel to the maturation of the myenteric nerve perikarya and dendrites. The early fetal period was marked by axonal growth cones. Regardless of the fact that during the development their frequency decreased at the expense of axon varicosities, growth cones were also observed in the first postnatal month. The formation of the axon varicosities was intensive in the late fetal period and in the first weeks after birth. This was judged from the changes in the volume fraction of the varicosities to total neuropil and the number of the varicosities per 100 sp x micrometer of neuropil. The maturation of the varicosities exhibited a longer course which was evident from the changes in the number of the vesicles and in the varicosity area. The cholinergic varicosities differentiated first and most quickly. The so-called p-type varicosities appeared as early as the fetal period, but their number continued to increase after birth. The adrenergic varicosities developed most slowly, which was confirmed by the experiments with 6-OHDA. The axons differentiated with a different speed in the three sphincters examined.

Aging↗
PubMed2004

Calbindin-immunopositive cells are cholinergic interneurons in the myenteric plexus of rabbit ileum.

The 28-kDa calcium-binding protein (calbindin) is a widely studied neuronal marker in the enteric nervous system of numerous species. Calbindin has previously been detected in myenteric neurons of rabbit ileum in which 3% of all myenteric neurons are calbindin-immunopositive. We have studied the detailed morphology and chemical coding of calbindin-immunopositive neurons in this segment of the gut. We have found calbindin immunoreactivity in both strongly and weakly stained neurons. Of these, the strongly immunoreactive neurons belong to the Dogiel type I category. These neurons project only to other ganglia and primary strands of the plexus and their processes never run to the muscle or mucosal layers. The neurons within this group are 29.5+/-6.6 microm in length and 14.7+/-3.8 microm in width. The second smaller group of immunoreactive cells (27%) label faintly and have different morphological properties. They are characterized by their round medium-sized cell bodies (long axis: 24.4+/-5.2 microm; short axis: 15.5+/-2.9 microm) and do not exhibit immunoreactivity either in their dendrites or in their axonal processes. Double-label studies show that all calbindin-immunopositive neurons lack immunoreactivity for nitric oxide synthase, vasoactive intestinal peptide and substance P but all are immunoreactive for the synthesizing enzyme of acetylcholine, choline acetyltransferase. Thus, populations of neurons containing calbindin are cholinergic interneurons in the myenteric plexus of rabbit ileum.

Animals↗
PubMed1988

Localization of muscarinic receptors on peptide-containing neurones of the guinea pig myenteric plexus in tissue culture.

A combined autoradiographic and immunocytochemical procedure has been used to identify neurochemically the subpopulation of cultured myenteric neurones which expresses muscarinic receptors. Antibodies to substance P (SP), [Met]enkephalin (ENK), vasoactive intestinal polypeptide (VIP) and somatostatin (SOM) were used to immunostain cultures that had previously been labelled with the irreversible muscarinic antagonist, [3H]propylbenzilylcholine mustard. Most neurites which displayed SP-like, ENK-like or SOM-like immunoreactivity did not possess muscarinic receptors. In contrast, many VIP-like immunopositive fibres also possessed muscarinic receptors. The identity of the majority of neurones which express muscarinic receptors, that do not contain VIP, remains to be determined.

Animals↗
PubMed2000

Evaluation of the areas of neuronal cell bodies and nuclei in the myenteric plexus of the duodenum of adult rats.

This study compared the areas of cell body and nucleus profiles of the myenteric neurons in the antimesenteric and intermediate regions of the duodenum of adult rats. Five male rats were used. The duodenum was removed and dissected to whole-mount preparations, which were stained by the Giemsa technique. The areas of cell body and nucleus profiles of 100 neurons, 50 from each region, of each animal, were assessed with image analyser. Based on the global mean+/-SD of the areas of cell body profiles, neurons were labelled as small, medium or large. It was observed that the neurons did not differ significantly in size or incidence between the antimesenteric and intermediate regions. However, the nuclei of the small and medium neurons were significantly smaller in the latter region. It is discussed that the smaller nuclear size could be related to the cell bodies being slightly smaller on this region and to a possible smaller biosynthetic activity which would influence nuclear size.

Animals↗