Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pattern of nerves, ganglia, and fine nerve processes in the adult rabbit sinoatrial node, identified by microelectrode recording, was defined by staining histochemically for cholinesterase followed by silver impregnation. A generalized repeatable pattern of innervation was recognized, including 1) a large ganglionic complex inferior to the sinoatrial node; 2) two or three moderately large nerves traversing the sinoatrial node parallel to the crista terminalis; 3) nerves entering the region from the atrial septum, the superior vena cava, and the inferior vena cava; and 4) a fine network of nerve processes, particularly extensive in the morphologically dense small-cell part of the sinoatrial node. When the site of initial depolarization in the node was located and marked by a broken-off electrode tip, it was found, after cholinesterase staining, to be characterized by a cluster of cells enclosed in a nest or basket of fine nerves. Similar nested cell clusters were observed elsewhere in the sinoatrial node in this same preparation and in other hearts. A complex interweaving of atrial muscle fibers was observed medial and inferomedial to the sinoatrial node, which may form the anatomical basis for the lack of conduction through this region. The morphological pattern of nerves, ganglia, and myocardial cells described in this study emphasizes the complexity of innervation of the sinoatrial node, including its intrinsic neural elements. Cholinesterase/silver staining can be useful in the definition and comparison of electrophysiologically identified sites within the sinoatrial node.
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PMID:Morphological study of the innervation pattern of the rabbit sinoatrial node. 278 78

The effects of a prolonged blockade of nerve conduction by tetrodotoxin on frog motor innervation were studied in the cutaneous pectoris muscle of Rana esculenta. Prolonged nerve blockade (up to 22 days) was obtained by repeated subperineural injections of tetrodotoxin. Changes in morphological parameters of neuromuscular junctions were investigated in muscles after staining with a combined cholinesterase-silver method. In addition, changes in the incidence of polyneuronal innervation were investigated conjointly by electrophysiology and morphology. Morphometric analysis of singly innervated muscle fibres of 60 microns diameter revealed insignificant changes during the first week of tetrodotoxin-nerve blockade. After 15 days of paralysis, the mean length of synaptic contacts and the mean length of terminal arborization per synapse were significantly increased as compared to controls (contralateral muscles and citrate buffer-injected controls). After 20-22 days, differences in synaptic and aborization mean lengths were accentuated and reached 44 and 43%, respectively. At that time, the mean number of terminal branching points and of continuous synaptic contacts were also significantly increased (around 20 and 50%, respectively). No changes in the length of abandoned gutters were observed. The incidence of focal polyaxonal innervation (detected morphologically) and of polyneuronal innervation (determined electrophysiologically) was unchanged. The results show that prolonged tetrodotoxin blockade induces sprouting of the terminal arborization which results in an extension of pre-existing nerve terminals and an increase in the complexity of terminal arborization by addition of new branches. Nodal (collateral) sprouting was not changed.
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PMID:Terminal nerve sprouting at the frog neuromuscular junction induced by prolonged tetrodotoxin blockade of nerve conduction. 278 62

The ability of axons to grow or sprout can vary considerably. In this study we have examined the relation between axon length and the abundance of outgrowth from motor nerve terminals in vivo. Outgrowth from nerve terminals was evoked using botulinum toxin. Terminal axons, sprouts and neuromuscular junctions were visualized using a cholinesterase-silver stain. The amount of axonal outgrowth was compared in several proximal (e.g. rhomboid and paraspinous), intermediate, and distal (e.g. soleus and foot) muscles. Our results show that sprouting is generally more abundant in proximal than in distal muscles. There is a significant inverse correlation between nerve length and the abundance of sprouting from terminal axons. Thus, terminals of short axons appear to have more ability or potential to sprout than those of long axons.
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PMID:Motor nerve outgrowth: reduced capacity for sprouting in the terminals of longer axons. 319 14

Motor nerve terminal outgrowth (NTO) at neuromuscular junctions (NMJs) occurs rapidly in response to denervation changes in muscle. We have previously found that NTO can produce an elongation of the synaptic area of the NMJ as defined by cholinesterase-silver staining. In the present study, we examined the effects of NTO on a postsynaptic muscle membrane component, the usually stable cluster of acetylcholine receptors (AChRs) at the NMJ. NTO was evoked in rat soleus muscles using botulinum toxin. AChRs were demonstrated using immunocytochemistry or autoradiography of alpha-bungarotoxin binding. Our results show that NTO induces rapid elongation of the cluster of AChRs at the NMJ within 7 d of treatment with botulinum toxin. The growth in the size of the AChR clusters was accompanied by an increase in the number of AChRs/NMJ. No elongation of AChR clusters was seen following surgical denervation, suggesting that cluster growth is related to NTO and not to denervation changes in muscle per se. Growth of NMJ-AChR clusters appeared to result primarily from 2 processes: insertion of new AChRs into the NMJ membrane and, surprisingly, redistribution of preexisting NMJ-AChRs. These results show that NTO can cause rapid changes in the normally stable cluster of AChRs at the NMJ. Motor nerve terminals provide a strong and anatomically precise control of AChRs at the NMJ.
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PMID:Mechanisms of postsynaptic plasticity: remodeling of the junctional acetylcholine receptor cluster induced by motor nerve terminal outgrowth. 330 23

The proportion of polyneuronal innervation was evaluated electrophysiologically in curare-blocked frog cutaneous pectoris muscles after local injury to the muscle fibres on one side. Focal polyneuronal innervation was revealed by recording end-plate potentials evoked by a gradual increase in the stimulus intensity applied to the motor nerve. An increase in the proportion of focally polyneuronally innervated muscle fibres appeared in the injured muscle 3-5 days after injury. The difference between the values obtained 3-5 days and 7-9 days (31 and 38%, respectively) and the control value (18%) was highly significant. A similar increase in the proportion of pluri-innervated muscle fibres was observed in the contralateral muscle, but after a longer period. The different components of complex end-plate potentials (e.p.p.s) usually had similar latencies and rise times in control and experimental muscles. This may indicate that the axons had similar conduction velocities and that synapses were located close to each other. A repeated muscle fibre section 24 h after the initial injury resulted in an enhanced polyneuronal innervation (52%) 7-9 days after the first section. The experiments were repeated on partially blocked muscles in order to detect small e.p.p.s with an amplitude similar to that of spontaneous miniature end-plate potentials (m.e.p.p.s). The proportion of polyneuronally innervated fibres estimated by this technique in control muscles approximated 40%. Polyneuronal innervation was also found to be significantly increased in cut muscles 7-9 days after muscle injury and a week later in contralateral muscles. Combined silver and cholinesterase staining was used to detect morphologically polyneuronal innervation. The comparison of morphological and electrophysiological data indicated that the increase in polyneuronal innervation after muscle injury is likely due to nerve sprouting and formation of new synapses. The results suggest that the signal for nerve sprouting originates from the damaged muscle cell and that it is transferred transneuronally to the contralateral side.
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PMID:Increase in polyneuronal innervation in frog muscle after muscle injury. 348 69

The identity of a peptidase activity with human serum pseudocholinesterase (PsChE) purified to apparent homogeneity was demonstrated by co-elution of both peptidase and PsChE activities from procainamide-Sepharose and concanavalin-A--Sepharose affinity chromatographic columns; comigration on polyacrylamide gel electrophoresis; co-elution on Sephadex G-200 gel filtration and coprecipitation at different dilutions of an antibody raised against purified PsChE. The purified enzyme showed a single protein band on gel electrophoresis under non-denaturing conditions. SDS gel electrophoresis under reducing conditions, followed by silver staining, also gave a single protein band (Mr approximately equal to 90,000). Peptidase activity using different peptides showed the release of C-terminal amino acids. Blocking the carboxy terminal by an amide or ester group did not prevent the hydrolysis of peptides. There was no evidence for release of N-terminal amino acids. Potent anionic or esterase site inhibitors of PsChE, such as eserine sulphate, neostigmine, procainamide, ethopropazine, imipramine, diisopropylfluorophosphate, tetra-isopropylpyrophosphoramide and phenyl boronic acid, did not inhibit the peptidase activity. An anionic site inhibitor (neostigmine or eserine) in combination with an esterase site inhibitor (diisopropylfluorophosphate) also did not inhibit the peptidase. However, the choline esters (acetylcholine, butyrylcholine, propionylcholine, benzoylcholine and succinylcholine) markedly inhibited the peptidase activity in parallel to PsChE. Choline alone or in combination with acetate, butyrate, propionate, benzoate or succinate did not significantly inhibit the peptidase activity. It appeared that inhibitor compounds which bind to both the anionic and esteratic sites simultaneously (like the substrate analogues choline esters) could inhibit the peptidase activity possibly through conformational changes affecting a peptidase domain.
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PMID:A peptidase activity exhibited by human serum pseudocholinesterase. 354 20

The mdx mutant mouse was first observed during a survey of genetic variations of pyruvate kinase in the mouse. Affected mice have high serum levels of this enzyme and although showing little disability they have widespread and severe muscle disease. Light and electron microscopy, muscle enzyme histochemistry and combined cholinesterase-silver impregnations were used for the study of affected and control animals aged 1 day to 1 year. An early ultrastructural abnormality present already at 1 day was scattered focal streaming of Z-lines. Later there was also segmental muscle fibre necrosis and regeneration. The proportion of muscle fibres showing either necrosis, regeneration or internal nuclei was assessed in several muscles, at ages ranging from 10 days to 1 year. Acute segmental necrosis and regeneration were most marked at 1 to 2 months, although they were present at all ages. The number of fibres with internal nuclei increased progressively until 3 months when 70-80% showed this abnormality. Nerve terminals were unaffected but there was a reduction in the number and depth of postsynaptic folds at motor end-plates in adult animals, confirmed by morphometric analysis. Quantitative study of L4 motor root and tibial nerve showed that fibre numbers, axonal calibres and myelin sheath thickness were normal at all ages. No qualitative abnormalities were found in the CNS or other organs. The findings strongly suggest that the mdx mutant has a primary muscle disease and that the nervous system is normal.
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PMID:The mutant mdx: inherited myopathy in the mouse. Morphological studies of nerves, muscles and end-plates. 356 25

This histochemical study examined the effects of chronic methylmercury (MeHg) intoxication on the motor and sensory innervation of extensor digitorum longus muscles. Light microscopic examination of silver-stained axons in the intramuscular nerve bundles of MeHg-treated rats showed Wallerian-like degeneration and a reduction in the number of nerve fibers. Disrupted axons were predominantly sensory because 22.2% of spindle afferents (Ia) and 90.0% of Golgi tendon organ (Ib) sensory fibers were completely degenerated whereas less than 1% of motor endings were totally destroyed. Partial disruption occurred in the cholinesterase and motor terminals of 13.7% of endplates. Our results demonstrated greater vulnerability of sensory nerves than of motor nerves to MeHg-induced degeneration. Thus, the abnormal reflexes, ataxia, and muscle weakness following MeHg poisoning appear related to reduction of proprioceptive feedback from muscles and tendons in addition to the documented lesions in the central nervous system.
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PMID:Effects of methylmercury on the motor and sensory innervation of the rat extensor digitorum longus muscle. 358 15

It's being studied through the technics of Koelle-Friedenwall for the detection of specific acetyl-cholinesterase, that of Champy-Maillet of tetroxide osmium-iodine of zinc and that of Jabonero's silver carbonate, the microganglions existing in pulmonary vessels. The attained results with Koelle-Friedenwall's technics were negative. With the other two technics we have observed small microganglions attached to the adventitial layer of pulmonary vessels, as much arteries and veins. In one case, we have realised the existence of a neuronal conglomerate inside the adventitial itself. They are formed by a scarce number of neurons, type I from Dogiel. We believe, due to its localization, that they are of a parasympathetic nature.
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PMID:[Innervation of the pulmonary vessels: autonomic microganglia]. 383 77

Motor nerves undergo extensive terminal outgrowth when the muscles they supply are "functionally denervated." In this study, we have investigated the role of the acetylcholine receptors (AChRs), newly appearing in such muscles, in promoting nerve terminal outgrowth. The amount of outgrowth was determined by morphometric measurement of nerve terminal branching, endplate length, and ultraterminal sprouts, in cholinesterase-silver-stained neuromuscular junctions. Presynaptic neuromuscular blockade with botulinum toxin induced pronounced nerve terminal outgrowth in both the rat and mouse soleus muscles, although ultraterminal sprouts did not occur in the rat soleus. By contrast, postsynaptic neuromuscular blockade with alpha-bungarotoxin (alpha-BuTx) induced little or no terminal outgrowth, although it caused "functional denervation." Moreover, alpha-BuTx and anti-AChR antibody inhibited the terminal outgrowth otherwise induced by botulinum toxin. Other types of motor nerve growth, such as nerve regeneration, were unaffected by these agents. Our results are consistent with the concept that extrajunctional AChRs in skeletal muscle play an important role in the control of motor nerve terminal outgrowth at neuromuscular junctions.
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PMID:Motor nerve terminal outgrowth and acetylcholine receptors: inhibition of terminal outgrowth by alpha-bungarotoxin and anti-acetylcholine receptor antibody. 387 42


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