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:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acetylcholine (ACh) is one of the factor which induces vasodilation through the release of endothelium-derived relaxing factor. The aim of this study was to clarify whether endothelial cells can synthesize ACh and the types of substance which regulate the synthesis of ACh in endothelial cells. We determined the ACh content of endothelial cells isolated from porcine cerebral microvessels and of the culture medium. ACh was detected in the medium after 12 h incubation in the presence of diisopropylfluorophosphate, a non-specific cholinesterase inhibitor, and increased linearly up to 24 h. Phorbol 12-myristate 13-acetate (PMA, 10(-7) M) increased the ACh content of the medium in a dose-dependent manner. The effect of PMA was most apparent between 12 and 24 h after treatment, and was inhibited by cycloheximide. Calphostin C, a specific inhibitor of protein kinase C (PKC), did not inhibit the effect of PMA. Dioctanoyl glycerol, a specific activator of PKC, did not increase the intracellular ACh content or the amount released into the culture medium. ACh synthesis was not inhibited by bromoacetylcholine, a specific inhibitor of choline acetyltransferase (ChAT). PMA treatment did not affect the specific activity of ACh synthesis in endothelial cells. These data show that endothelial cells are able to synthesize ACh, and that ACh synthesis is up-regulated by PMA through the PKC independent mechanism via protein induction. The enzyme which synthesizes ACh in endothelial cells is not ChAT. The increase in ACh synthesis induced by PMA may not be due to induction of the ACh synthetic enzyme.
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PMID:Phorbol ester stimulates acetylcholine synthesis in cultured endothelial cells isolated from porcine cerebral microvessels. 752 25

The levels of neurotransmitters and related metabolic enzyme activities in the brain of young-adult (3 months old), aged (11 months old) and nimodipine-administered (11 months old) senescence-accelerated mouse (SAM) were compared. Nimodipine, a calcium antagonist, was administered orally for 5 months. Acetylcholine (ACh), serotonin (5-HT) and dopamine (DA) levels all decreased with age but this decrease was attenuated by nimodipine. Choline acetyltransferase and choline esterase activities increased with age, and nimodipine enhanced their activities. Tryptophan hydroxylase activity was not affected by age or nimodipine administration. Monoamine oxidase-A activity increased with age, and was decreased by nimodipine administration. These results suggest that SAM rapidly undergoes neurochemical changes which are considered to be part of the normal aging process, and these changes were attenuated by chronic administration of nimodipine.
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PMID:Neurochemical changes related to ageing in the senescence-accelerated mouse brain and the effect of chronic administration of nimodipine. 756 56

In cases of colorectal innervation disturbance the histological and histochemical findings are well placed to classify the morphological state and to indicate to the pediatric surgeon the therapeutic direction. Any limitation of their value results from technical errors, age dependent localization of morphological structures and the subjectivity of the assessment. For this reason a quantitative biochemical investigation of cholinesterase activity in homogenized investigation of cholinesterase activity in homogenized rectal mucosa specimens and resected bowel segments was performed. The biochemical standard value of the AChE-activity amounts up to 3-6 x 10(-7) mol ACh/min/g in healthy test patients and the ratio of specific/unspecific esterases 1.1 to 1.3. The percentage of AChE to the total enzyme activity was 47.5%. The standard distribution of the different globular and asymmetric cholinesterase structures is described by the proportion of the molecular types G1/G2/G4 and A12. These main types determine the biochemical nature of the human rectum. Hypertrophy of cholinergic nerve fibres in aganglionic bowel segments correlates pathobiochemically with the increase of the cholinesterases caused by the high molecular tetramer G4. However, the Hirschsprung's disease could not be differentiated by the percentage of the AChE-activity to the total ChE-activity because of the continuous increase in the BChE in the aganglionic tissue. Neuronal intestinal dysplasias with their main cholinergic nerve fibre hyperplasias are characterized by disturbances of the dualism and interrelation of different cholinesterases. By means of pathogiochemical investigations the subjective factor in the assessment of histochemical states is avoided and the diagnostic accuracy increased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantitative investigations of acetylcholinesterase activities in colorectal malformations. 774 35

1. The physiology and pharmacology of the connections made by stress-sensitive campaniform sensilla on the proximal dorsal tibia of a locust hind leg with a fast extensor tibiae motor neuron (FETi) have been examined. 2. Mechanical stimulation of a campaniform sensillum on the anterior surface of the tibia elicited bursts of spikes in its afferent and a depolarization in FETi. Each afferent spike was followed at short and constant latency by an excitatory postsynaptic potential (EPSP) in FETi, even at high-frequency stimulation. Electrical stimulation of the extensor tibiae muscle with the tibia fixed elicited an antidromic spike in FETi followed by a compound potential which resulted from the activation of the campaniform sensillum afferent. The connections between the campaniform sensillum and FETi was monosynaptic and chemically mediated. 3. Ionophoresis of ACh into the neuropil depolarized FETi, as did the application of the cholinesterase inhibitor physostigmine. Bath application of the cholinergic agonists, nicotine and muscarine, also depolarized FETi, with nicotine causing a reduction in input resistance, while muscarine caused no detectable change in input resistance. Muscarine and the muscarinic agonist oxotremorine also caused rhythmic depolarizations and bursts of spikes in FETi. These effects were seen in low calcium/high magnesium saline to block synaptic transmission and are therefore due to direct effects on FETi. FETi therefore appears to have both nicotinic and muscarinic receptors. 4. The compound potential in FETi, caused by activation of the campaniform sensillum, was reduced by bath application of nicotinic cholinergic antagonists. However, the muscarinic antagonist scopolamine increased the amplitude of the compound potential.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cholinergic synaptic transmission between proprioceptive afferents and a hind leg motor neuron in the locust. 776 Jan 20

Acetylcholine (ACh) acts on the pulmonary vasculature to evoke vasodilation and, in some species, vasoconstriction. The actions of ACh are terminated by its rapid hydrolysis by cholinesterases. Aside from histochemical localization studies, there is little information on cholinesterase enzymes in pulmonary blood vessels. The present study addresses the hypothesis that pulmonary blood vessels contain sufficient cholinesterase activity to regulate the action of ACh in these tissues. Accordingly, studies were undertaken to characterize and quantify cholinesterase activities in pulmonary arteries and veins, quantify inhibition of enzyme activity, and investigate functional physiological consequences of cholinesterase inhibition. Cholinesterase activities in aorta and trachea also were examined for comparison. Kinetic studies showed that the lobar pulmonary arterial enzyme has a Michaelis constant of 55.3 +/- 17.0 microM and a maximum velocity of 8.6 +/- 2.7 nmol/min/mg protein similar to cholinesterases found in other peripheral tissues. Studies with selective inhibitors revealed that > 98% of total enzyme activity was attributable to acetylcholinesterase. Similar levels of enzyme activity were found in homogenates of lobar branch intrapulmonary arteries, intrapulmonary veins, and aorta. The majority of enzyme activity was localized to the membrane fraction, although a moderate amount was found in the cytosol. Studies in intact intrapulmonary lobar arteries showed that these vessels had cholinesterase activity comparable with that found in intact trachealis muscle and that neostigmine (10 nM to 10 microM) caused concentration-dependent inhibition of enzyme activity. In isolated intrapulmonary lobar arteries, functional studies showed that 1 and 10 microM neostigmine significantly potentiated ACh-induced contractions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of acetylcholinesterase in rabbit intrapulmonary arteries. 781 Jun 79

Acetylcholine, acetylthiocholine, carbachol, suberyldicholine, propionylcholine, succinylcholine, methylfurmethide and F 2268 were tested on motor nerve ending currents recorded with an extracellular microelectrode. The isolated and transversally cut cutaneous pectoris muscle of frog Rana ridibunda was used. Only acetylcholine and acetylthiocholine affected the spike waveforms in a concentration-dependent manner. Lower concentrations (1-6 x 10(-4) M) prolonged the inward Na+ current and increased the outward K+ current at the proximal and central parts of the nerve terminal. Most remote parts of the terminal were not affected. At 7 x 10(-4) M and higher, both drugs further prolonged the Na+ current and eliminated the K+ component of the spike. The potentiating effect of acetylcholine and acetylthiocholine on the K+ phase of nerve terminal current disappeared after treatment with tetraethylammonium and 4-aminopyridine. The effect also disappeared when synaptic cholinesterase was inhibited by the anticholinesterases or by treatment with collagenase. Reactivation of cholinesterase by dipyroxime restored the facilitating effect of acetylcholine. Choline and slight acidification to pH 6.8 did not mimic the acetylcholine action on the terminal currents. Facilitation of the K+ current by acetylcholine was not calcium-dependent. The results indicate that lower acetylcholine concentrations inhibit the delayed rectifier only, whereas 7 x 10(-4) M and higher concentrations of acetylcholine depress all outward currents of the terminal.
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PMID:The effect of acetylcholine and related drugs on currents at the frog motor nerve terminal. 782 42

Neurotransmitters have been reported to regulate neurite outgrowth in several vertebrate and nonvertebrate species. In this study, cultures of isolated embryonic day 12 (E12) chick sympathetic neurons were grown in the presence of cholinergic receptor agonists or antagonists. Both ACh and the nonhydrolyzable cholinergic agonist carbamylcholine (CCh) inhibited neurite outgrowth. ACh (0.1-1.0 mM) decreased the percentage of neurons bearing neurites, but had no significant effect on cell survival. The effect of ACh was increased in the presence of the cholinesterase inhibitors BW284C51 (1 microM), Tacrine (20 microM), and edrophonium (200 microM). Neurite outgrowth was strongly inhibited by the muscarinic receptor agonist oxotremorine (5-100 microM) and weakly inhibited by nicotine (50 nM to 10 microM). The inhibitory effect of CCh was decreased by the muscarinic receptor antagonist atropine (10 microM), demonstrating that the effect of CCh on neurite outgrowth was mediated, at least in part, through a muscarinic receptor. The possibility that AChE can influence neurite outgrowth directly, through a noncatalytic mechanism, was also examined. When dissociated chick brain or sympathetic neurons were grown on plates precoated with purified AChE, neurite outgrowth was strongly stimulated. However, the neurite outgrowth-promoting effect of AChE was strictly dependent upon the presence of substratum-bound heparan sulfate proteoglycans (HSPG). Pretreatment of AChE with diisopropylfluorophosphate to inhibit the esterase activity did not abolish this effect, suggesting that the neurite outgrowth-promoting effect of AChE was associated with a noncatalytic mechanism, a view supported by the observation that soluble AChE had no effect on neurite outgrowth.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cholinergic regulation of neurite outgrowth from isolated chick sympathetic neurons in culture. 782 25

Acetylcholine (ACh) and choline (Ch) levels in rat cerebrospinal fluid (CSF) were determined by in vivo microdialysis (CSF microdialysis) in both halothane-anesthetized and freely-moving rats. The Ch/ACh ratio in CSF perfused with Ringer's solution (30 microliters/30 min) containing 10(-5) M physostigmine, a centrally active cholinesterase inhibitor, was significantly lower than that in unprocessed CSF due to significantly higher ACh levels in the former. The successive measurement on the 2nd and 7th day after the guide cannula implantation demonstrated the feasibility of the CSF microdialysis method for repetitive monitoring of CSF ACh and Ch levels in freely moving rats without extensive tissue damage. Intraperitoneal administration of physostigmine caused an increase in CSF ACh levels, whereas administration of neostigmine, which cannot penetrate into the blood brain barrier, did not. Furthermore, a centrally active acetylcholinergic M1-receptor agonist, AF102B, produced an increase in CSF ACh and Ch levels. Thus, the present study demonstrates that CSF microdialysis is a useful method for evaluating overall central cholinergic activity and investigating the pharmacological effects of various drugs that act via the central cholinergic system.
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PMID:Acetylcholine measurement of cerebrospinal fluid by in vivo microdialysis in freely moving rats. 786 69

The effects of a subacute intoxication with diisopropyl fluorophosphate (DPF) on total muscarinic acetylcholine receptor sites (mAChRs) and M-1 AChRs were evaluated in the cerebral cortex of young (2-4 months) and aged (22-24 months) Fischer 344 rats. Since M-1 AChRs are coupled to the metabolism of phosphoinositides, carbachol-induced accumulation of inositol phosphates (IP) and its inhibition by glutamate and NMDA was also measured in the cortical slices. DFP treatment caused about 75% inhibition of cholinesterase and 35% down-regulation of mAChRs (measured as [3H]quinuclidinyl benzylate binding) in both young and aged rats. The down-regulation of M-1-ACHRs (measured as [3H]pirenzepine binding) was more pronounced in aged (30%) than in young (17%) DFP-treated rats. There was a significant increase in carbachol-induced IP accumulation in aged, with respect to young, untreated rats. DFP treatment caused a considerable decrease in such IP accumulation in aged but not in young rats. Glutamate and NMDA antagonized carbachol-induced IP accumulation in untreated young and aged rats (and the effects of NMDA were reversed by carboxy-piperazinyl-propyl phosphonic acid). In DFP-treated rats such antagonism was somewhat less pronounced. The data appear of interest in relation to the use of anticholinesterase compounds in the therapy of senile dementia of Alzheimer's type. They suggest that beside their primary action (increasing brain ACh levels) such compounds also act on post-receptor mechanisms and on the interactions between cholinergic and glutamatergic neurotransmitter systems.
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PMID:Carbachol-induced accumulation of inositol phosphates and its modulation by excitatory amino acids in cortical slices of young and aged rats with down-regulation of muscarinic M-1 receptors. 789 49

1. Both butyrylcholinesterase (BChE) and acetylcholinesterase (AChE) are present in the mouse uterus, BChE being more abundant. 2. Their molecular forms were sequentially solubilized by different extraction media obtaining three ChE fractions whose specific activity was different, depending on the stage of the estrous cycle: hydrosoluble (estrous: 75.5 +/- 6.6 and diestrous: 47.9 +/- 8.7 mU/mg prot); detergent-soluble or amphiphilic (estrous 26.6 +/- 2.4 and diestrous 14.7 +/- 3.3 mU/mg prot.), and high ionic strength-soluble (estrous: 18.7 +/- 4.2 and diestrous 12.8 +/- 1.2 mU/mg prot.). 3. Histochemical procedures demonstrated a different distribution for both ChE activities. AChE was found in nerves next to smooth muscle cells of the circular layer and blood vessels, while BChE was concentrated in the longitudinal stratum surrounding the smooth muscle cells. Under the predominance of progesterone, BChE was also found in the endometrial glands. 4. Maximal contractions evoked by the addition of ACh to the isolated organ bath were concentration dependent and greater in estrous than in diestrous. Nevertheless the difference at the two stages of the estrous cycle disappeared when contractions were normalized to smooth muscle cross-sectional area. 5. BChE but not AChE inhibition augmented maximal contractions elicited by ACh in longitudinal but not in circular smooth muscle. 6. The effect of BChE inhibition on the contractile force developed was greater at lower concentrations of ACh and did not depend on the stage of the estrous cycle.
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PMID:Characterization and distribution of cholinesterase activity in mouse uterine horns: changes in estrous cycle. 790 19


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