Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.7 (acetylcholinesterase)
28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pancreatic islets transplanted to the kidney of syngeneic mice were stained for calcitonin gene-related peptide (CGRP), substance P (SP), tyrosine hydroxylase (TH), acetylcholinesterase and the pan-neuronal marker, protein gene product 9.5 (PGP). Nerve fibers expressing TH-like immunoreactivity (TH-LI) and CGRP-LI were rare for 4 days but increased 2 (CGRP) or 6 (TH) weeks after transplantation. In 1-year-old grafts the CGRP-LI innervation resembled that in situ, while TH-LI and PGP-LI innervations were increased. SP-LI fibers remained rare throughout. Perikarya intrinsic to the islets did not show CGRP-LI or SP-LI. The results indicate a progressive ingrowth of sensory fibers into the grafts and that the TH-LI innervation becomes even more pronounced than in the pancreas. The post-transplantation reaction of islet intrinsic neurons does not involve CGRP and SP, contrasting with previous observations for vasoactive intestinal polypeptide.
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PMID:Expression of tyrosine hydroxylase, calcitonin gene-related peptide, substance P and protein gene product 9.5 in mouse islets transplanted under the kidney capsule. 1010 75

A homozygous CGRP-/- mouse line was generated by the targeted disruption of exon 5 in the calcitonin/alphaCGRP gene using homologous recombination. The mutant mice lack alphaCGRP mRNA. Furthermore CGRP immunoreactivity almost completely disappears from the spinal cord and is not at all observed in spinal ganglia and muscle synapses. However, motor end plates were still detected by acetylcholinesterase staining. Antinociceptive behavior tested by the tail flick and hot plate tests did not significantly differ in mutant and wild-type mice, except when challenged by morphine. Paradoxically, morphine analgesia was reduced in mutant mice compared with controls in the tail flick test, but not in the hot plate test. Thus, alphaCGRP differentially modulates opiate pain pathways.
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PMID:Modulation of morphine analgesia in alphaCGRP mutant mice. 1020 59

Thirty mouse monoclonal antibodies (mAbs) directed against rat calcitonin gene-related peptide-alpha (CGRP-alpha) have been obtained. These mAbs are classified in 2 groups, one recognizing the peptide N-terminus and the other binding the C-terminus. A two-site immunometric assay was developed using mAb CGRP-83 as capture antibody, whereas mAb CGRP-72 acts as tracer, covalently labeled with enzyme acetylcholinesterase. This assay appeared sensitive (limit of detection: 2 pg/ml) and precise, allowing quantitative measurement of all human and murine CGRP isoforms. The assay was used to determine specific concentrations of CGRP in different rat, mice and guinea pig samples. The validity of the test was demonstrated by HPLC fractionation experiments.
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PMID:A sensitive sandwich enzyme immunoassay for calcitonin gene-related peptide (CGRP): characterization and application. 1042 84

This work addresses the role of calcitonin gene-related peptide (CGRP) in the physiological maintenance of acetylcholinesterase (AChE) molecular forms in motor endplate regions of adult Sprague-Dawley rat fast-twitch anterior gracilis muscles. Results show that: (a) CGRP is present in obturator nerve motor neurons which supply the gracilis muscle, as well as in the corresponding motor endplate regions where high levels of both AChE activity and acetylcholine receptors (AChRs) are detected; (b) endplate-associated CGRP declines with muscle denervation several hours before any changes in AChE forms are detected; (c) a single subcutaneous injection of CGRP reversibly reduces the activities of all AChE forms in endplate regions of normally innervated and otherwise untreated gracilis muscles; and (d) similar treatment with hCGRP(8-37), a potent and selective CGRP antagonist, produces the opposite effects, i.e., it reversibly elevates the activities of all AChE forms. These and other findings indicate that CGRP and hCGRP(8-37) influence the mechanism(s) by which AChE forms are maintained in intact adult gracilis muscles. Indeed, the findings lend strong support to the hypothesis that nerve-derived CGRP plays a key role in the trophic regulation of AChE forms at the neuromuscular junction.
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PMID:Neurogenic calcitonin gene-related peptide: a neurotrophic factor in the maintenance of acetylcholinesterase molecular forms in adult skeletal muscles. 1053 64

Adhesions in the peritoneal cavity have been implicated in the cause of intestinal obstruction and infertility, but their role in the aetiology of chronic pelvic pain is unclear. Nerves have been demonstrated in human pelvic adhesions, but the presence of pain-conducting fibres has not been established. The purpose of this study was to use an animal model to examine the growth of nerves during adhesion formation at various times following injury and to characterize the types of fibres present. Adhesions were generated in mice by injuring the surface of the caecum and adjacent abdominal wall, with apposition. At 1-8 weeks post-surgery, adhesions were processed and nerve fibres characterized histologically, immunohistochemically, and ultrastructurally. Peritoneal adhesions had consistently formed by 1 week after surgery and from 2 weeks onwards, all adhesions contained some nerve fibres which were synaptophysin, calcitonin gene-related peptide, and substance P-immunoreactive, and were seen to originate from the caecum. By 4 weeks post-surgery, nerve fibres were found to originate from both the caecum and the abdominal wall, and as demonstrated by acetylcholinesterase histochemistry, many traversed the entire adhesion. Ultrastructural analysis showed both myelinated and non-myelinated nerve fibres within the adhesion. This study provides the first direct evidence for the growth of sensory nerve fibres within abdominal visceral adhesions in a murine model and suggests that there may be nerve fibres involved in the conduction of pain stimuli.
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PMID:Growth of nerve fibres into murine peritoneal adhesions. 1105 24

The gut of silver eels (Anguilla anguilla L.) was investigated in order to describe both the cholinergic and adrenergic intramural innervations, and the localization of possible accessory neuromediators. Histochemical reactions for the demonstration of nicotinamide adenine dinucleotide phosphate, reduced form-(NADPH-)diaphorase and acetylcholinesterase (AChEase) were performed, as well as the immunohistochemical testing of tyrosine hydroxylase, met-enkephalin, substance P, calcitonin gene-related peptide (CGRP), bombesin, vasoactive intestinal peptide (VIP), neuropeptide Y (NPY), somatostatin, cholecystokinin-octapeptide (CCK-8), serotonin, cholineacetyl transferase. The results evidenced a different pattern in comparison with other vertebrates, namely mammals, and with other fish. Both NADPH-diaphorase and AChEase activities were histochemically detected all along the gut in the myenteric plexus, the inner musculature and the propria-submucosa. Tyrosine hydroxylase immunoreactivity was observed in the intestinal tract only, both in the myenteric plexus and in the inner musculature. Several neuropeptides (metenkephalin, CGRP, bombesin, substance P, VIP, NPY, somatostatin) were, in addition, detected in the intramural innervation; some of them also in epithelial cells of the diffuse endocrine system (met-enkephalin, substance P, NPY, somatostatin). Serotonin was only present in endocrine cells. Tyrosine hydroxylase immunoreactivity was present in localizations similar to those of NADPH-diaphorase-reactivity, and in the same nerve bundles in which substance P- and CGRP-like-immunoreactivities were detectable in the intestinal tract. In addition, NADPH-diaphorase-reactive neurons showed an anatomical relationship with AChEase-reactive nerve terminals, and a similar relationship existed between the latter and substance P-like immunoreactivity.
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PMID:Neurotransmitters and putative neuromodulators in the gut of Anguilla anguilla (L.). Localizations in the enteric nervous and endocrine systems. 1109 1

The motility of the avian oviduct is controlled by hormones and neurons, but little is microscopically known about a neural network in the oviduct. The present study was investigated to determine the distribution of nitric oxide-synthesizing neurons in the oviduct of the pigeon by histochemistry for nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d). The NADPH-d reaction was seen in the neurons and fibers. NADPH-d neurons were mainly distributed around the arterioles of the intermuscular tissue in the upper oviduct (infundibulum, magnum, and isthmus); in addition, NADPH-d neurons were also seen in the smooth muscle layers and lamina propria in the lower oviduct (uterus and vagina). NADPH-d neurons were found singly or in small groups of two-eight cell bodies. The number of NADPH-d neurons was smallest in the infundibulum, gradually increased toward the vagina. NADPH-d was also shown to be strongly positive in many neurons in the ganglia of the vaginal adventitia. Bundles of NADPH-d fibers ran in the smooth muscle layer, surrounded blood vessels, or connected with small groups of NADPH-d neurons by forming strands. Thin fibers branched from these bundles and constituted a finer network in the smooth muscle layer and lamina propria. Acetylcholinesterase staining in neurons and fibers showed a similar pattern of NADPH-d distribution in the oviduct. By double staining, 70 approximately 77% of neurons showed colocalization of NADPH-d and acetylcholinesterase in the uterus and vagina. Tyrosine hydroxylase immunoreactivity stained only nerve fibers and were distributed largely around blood vessels in the oviduct. Nerve fibers immunoreactive for calcitonin-gene related peptide, galanin, methionine-enkephalin, substance P, or vasoactive intestinal peptide were found sparsely in the oviduct. These results demonstrate that nitrergic neurons make up a large subpopulation of intrinsic neurons that are closely associated with a cholinergic system in the pigeon oviduct, thus suggesting that nitric oxide and acetylcholine could be used to modify the relaxation of the avian oviduct.
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PMID:Innervation of the pigeon oviduct: correlation of NADPH diaphorase with acetylcholinesterase, tyrosine hydroxylase, and neuropeptides. 1110 84

The motility of the avian cloaca is under neural control, but little is known about the neural network that accomplishes this function. This present study was designed to determine the distribution of nitric oxide-synthesising neurons in the pigeon cloaca by enzyme histochemistry for reduced nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d). NADPH-d-positive staining was seen in the neurons and fibres in the cloaca. The highest density of nerve fibres was noted in the coprodeum and the lowest in the proctodeum. In the coprodeum, NADPH-d neurons were found singly, formed small groups of 2-10 neurons, or were seen in plexuses in the muscle layer, lamina propria, or around the arterioles. Several NADPH-d-positive neurons were also observed in the ganglia of the cloaca. NADPH-d fibres ran in the muscle layer, lamina muscularis mucosae and lamina propria, or surrounded blood vessels. The distribution pattern of acetylcholinesterase (AChE)-stained neurons and fibres in the cloaca was similar to that of NADPH-d. Double staining for NADPH-d and AChE showed colocalisation of the 2 enzymes in many neurons of the cloaca. Tyrosine hydroxylase (TH)-immunoreactive nerve fibres originating outside the cloaca were also noted. In the urodeum and proctodeum, neurons or fibres positive for NADPH-d, AChE or TH were scattered in the lamina propria. Nerve fibres immunoreactive for calcitonin-gene related peptide, galanin, methionine-enkephalin, substance P, and vasoactive intestinal peptide were found sparsely in the cloaca. Our results demonstrate that nitrergic neurons constitute a subpopulation which is closely associated with the cholinergic system in the pigeon cloaca.
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PMID:Innervation of NADPH diaphorase-containing neurons correlated with acetylcholinesterase, tyrosine hydroxylase, and neuropeptides in the pigeon cloaca. 1127 43

The present study analyses the short- (15 min - 2 h) and long-term (24 - 48 h) influences of calcitonin gene-related peptide (CGRP) on acetylcholinesterase (AChE) expression in the rat cultured skeletal muscle and the signal transduction events underlying CGRP actions. To assess the effect of CGRP on AChE synthesis, myotubes were pre-exposed to the irreversible AChE inhibitor diisopropyl fluorophosphate (DFP) and treated with CGRP or forskolin, an adenylyl cyclase (AC) activator. Treatment of myotubes with 1 - 100 nM CGRP for 2 h increased by up to 42% the synthesis of catalytically active AChE with a parallel increase in the intracellular cyclic AMP. The stimulation of AChE synthesis induced by CGRP was mimicked by direct activation of AC with 3 - 30 microM forskolin. In contrast, pre-treatment of cultures with 100 nM CGRP for 20 h reduced by 37% the subsequent synthesis of AChE, resulting in a 15% decrease in total AChE activity after 48 h CGRP treatment. Moreover, 24 h treatment of myotubes with 100 nM CGRP reduced by 54% the accumulation of cyclic AMP induced by a subsequent CGRP treatment. These findings indicate that, in skeletal muscle cells, CGRP modulates the AChE expression in a time-dependent manner, initially stimulating the enzyme synthesis through a cyclic AMP-dependent mechanism. The decreased AChE synthesis observed after long-term CGRP treatment suggests that CGRP signalling system is subject to desensitization or down-regulation, that might function as an important adaptative mechanism of the muscle fibre in response to long-term changes in neuromuscular transmission.
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PMID:Short- and long-term influences of calcitonin gene-related peptide on the synthesis of acetylcholinesterase in mammalian myotubes. 1135 Aug 58

Activation of microglia is among the first cellular changes in the injured CNS. However, little is known about their specific contribution to secondary damage or repair processes in neighboring neurons and nonneuronal cells or to the immune surveillance of the damaged tissue. Animal models with defective microglial response such as osteopetrosis provide an approach to explore these effects. Osteopetrosis (op) is an autosomal recessive mutation with a complete deficiency of the macrophage-colony stimulating factor (MCSF; CSF-1), an important mitogen for brain microglia. In the current study we examined the effects of this MCSF deficiency on the microglial reaction and the overall cellular response to nerve injury in the mouse axotomized facial motor nucleus. In the brain, MCSF receptor immunoreactivity was found only on microglia and was strongly up-regulated following injury. MCSF deficiency led to a failure of microglia to show a normal increase in early activation markers (thrombospondin, MCSF receptor, alpha M beta 2- and alpha 5 beta 1-integrins), to spread on the surface of axotomized motoneurons, and to proliferate after injury. Early recruitment of CD3(+) T-lymphocytes to the facial nucleus 24 hours after injury was reduced by 60%. In contrast, the neuronal and astrocyte response was not affected. There was a normal increase in the neuropeptides calcitonin gene-related peptide and galanin, neuronal c-JUN, and NADPH-diaphorase and a decrease in choline acetyltransferase and acetylcholinesterase. Astrocyte glial fibrillary acidic protein immunoreactivity also showed a normal increase. There was a normal influx of macrophages and granulocytes into the injured facial nerve. Synaptic stripping, neuronal survival, and speed of axonal regeneration were also not affected. The current results show a strong, selective effect of MCSF on the early activation of microglia and, indirectly, on lymphocyte recruitment. This early phase of microglial activation appears not to be involved in the process of repair following peripheral nerve injury. However, it is important in the initiation of inflammatory changes in the brain and in the interaction with the immune system.
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PMID:Microglia and the early phase of immune surveillance in the axotomized facial motor nucleus: impaired microglial activation and lymphocyte recruitment but no effect on neuronal survival or axonal regeneration in macrophage-colony stimulating factor-deficient mice. 1143 23


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