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)

Serotonin was found to inhibit human erythrocyte and electric-eel acetylcholinesterase activities. The serotonin amino group, free of negative charges in its vicinity and its hydroxyl group, were important for the inhibition. Serotonin precursors and several related compounds had little or no effect. Human plasma cholinesterase was also inhibited by serotonin and tryptamine. In contrast to these animal enzymes, the cholinesterase of Pseudomonas aeruginosa was refractory to serotonin and its derivatives under the same experimental conditions.
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PMID:Comparative study of the sensitivity of acetylcholinesterases and cholinesterases from animal and bacterial sources to inhibition by serotonin and its derivatives. 10 Mar 43

Quipazine (30 mg/kg i.p., 60 min), a serotonin-like drug increased ACh levels in the striatum (37%) but was without effect on the transmitter content in the hippocampus and the parietal cortex of the rat. Added in vitro(10(-5) M) or injected in vivo, quipazine did not affect choline acetylase and cholinesterase activities in striatal tissue. The drug effect on striatal ACh levels did not appear to be related to an interaction with dopamine metabolism. Indeed quipazine still increased striatal ACh levels after degeneration of the dopaminergic neurons had been induced by local injection of 6-OH-DA. p-Chlorophenylalanine (PCPA) pretreatment (300 mg/kg, 48 and 24 h before the experiment) definitely prevented the quipazine effect on ACh levels. This result suggested that the drug may partially act by its interference with 5-HT metabolism. 5-Methoxy-N,N-dimethyltryptamine (10 mg/kg, i.p., 30 min), a serotonergic agonist, induced a weak but significant increase in ACh levels. These data provide some preliminary evidence for the existence of an inhibitory control of the cholinergic interneurones by the serotonergic neurones projecting to the striatum. However, the lack of effect of 5-hydroxytryptophan (100 mg/kg i.p.), PCPA (2 x 300 mg/kg i.p.) and of Lilly 110 140 (10 mg/kg i.p.) and chlorimipramine (10 mg/kg i.p.), two potent inhibitors of 5-HT uptake, on striatal ACh levels indicate that further experiments are required to retain this hypothesis.
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PMID:Effect of quipazine, a serotonin-like drug, on striatal cholinergic interneurones. 13 94

To examine the effect of spasmogens on propulsive motility in the intestine, cathartic activity of drugs was investigated. Mice, rats and guinea pigs were individually observed in cages with 20 separate small rooms in which a sheet of filter paper covered the botton of case for observation of feces. The effect was evaluated 1 hr after drug administration. Cathartic activity of spasmogens was the most marked in mice followed by rats, but was rarely observed in guinea pigs. Cholinergic drugs and cholinesterase inhibitors had a cathartic effect in mice and rats, but the activity differed. Drugs such as acetylcholine and physostigmine produced a low cathartic activity even at sublethal and lethal doses. Other drugs as bethanechol, pilocarpine and neostigmine had a dose dependent cathartic effect at doses below lethal ones and were found to be clinically useful for intestinal relaxation after laparotomy. Among autacoids which contract the intestine by direct action on smooth muscles, histamine and bradykinin had no cathartic effect in mice and rats. 5-HT and prostaglandin E2 were dose dependent with a marked cathartic effect in both species. 5-HTP produced the same cathartic activity as that seen with 5-HT in mice, but had no cathartic effect in rats. The cathartic effect of BaCl2 was low, but dose dependent in both species. We recommend this method for the study of the effect of various compounds on the propulsive motility of the intestine.
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PMID:[Cathartic activity of spasmogens in mice, rats and guinea pigs (author's transl)]. 53 25

On the basis of structural relationships between 5-hydroxytryptamine (5-HT, serotonine) and eserine, the effect of 5-HT on partially purified brain cholinesterase (ChE) was studied. The addition of 5-HT to brain ChE in vitro resulted in its inhibition, and the constants characterizing this inhibition, namely, the inhibition rate ki (5.44 X 10(2) mol-1/l - min-1), the equilibrium constant K (1.86 X 10(-3), and the rate constant for spontaneous reactivation kr (1.01 min-1) were determined. The inhibition of AChE by 5-HT in vitro was found to be of the competitive type.
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PMID:Inhibition of cholinesterase by 5-hydroxytryptamine. 124 80

The effects of five cholinesterase inhibitors on forebrain monoamine and their metabolite levels, and on forebrain and plasma cholinesterase (ChE) activity in rat were studied in acute and chronic conditions. Acute tetrahydroaminoacridine (THA) dosing caused lower brain (68%) and higher plasma (90%) ChE inhibition than the other drugs studied and increased levels of brain dihydroxyphenylacetic acid (DOPAC) (236%), homovanillic acid (HVA) (197%) and 5-hydroxyindoleacetic acid (5-HIAA) (130%). Acute physostigmine (PHY) administration caused a 215% increase in brain DOPAC content. Despite high brain ChE inhibition induced by metrifonate (MTF), dichlorvos (DDVP) or naled no changes in brain noradrenaline (NA), dopamine (DA) or serotonin (5-HT) occurred due to treatment with the study drugs in the acute study. In the chronic 10-day study THA or PHY caused no substantial ChE inhibition in brain when measured 18 hours after the last dose, whereas MTF induced 74% ChE inhibition. Long-term treatment with THA or MTF caused no changes in monoamine levels, but PHY treatment resulted in slightly increased 5-HT values. These results suggest that MTF, DDVP and naled seem to act solely by cholinergic mechanisms. However, the central neuropharmacological mechanism of action of THA and PHY may involve changes in cholinergic as well as dopaminergic and serotoninergic systems.
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PMID:Effect of acute and chronic cholinesterase inhibition on biogenic amines in rat brain. 171 Nov 62

Stimulation of mucosal alkaline secretion represents an opportunity for discovering novel drugs of potential benefit in maintenance therapy of duodenal ulcer disease. We screened over 200 agents representing the full spectrum of pharmacological categories in order to characterize stimulatory pathways and identify mechanistic leads. A variety of eicosanoids, phospho-diesterase inhibitors and adrenoreceptor agonists together with forskolin, 6-hydroxy-dopamine, 2-chloroadenosine, diazepam, testosterone, dipyridamole and dihydropyridazinone caused a reproducible increase in the metabolism-dependent component of alkaline secretion in bullfrog proximal duodenum. PGE2 (ED50 0.02 microgram/ml) was the most potent agent in vitro and was also the most effective stimulant of duodenal alkalinization in vivo in an anaesthetized cat preparation. Agents without effect on spontaneous alkaline secretion by amphibian duodenum included agonists and antagonists of histamine, 5-hydroxy-tryptamine, gamma-aminobutyric acid, dopamine, muscarinic and nicotinic receptors, inhibitors of amine uptake, monoamine oxidase and cholinesterase, plus various corticoids, diuretics, oestrogens, chemotherapeutic (anticancer) and antimicrobial agents. The major mechanism of stimulating alkaline secretion in the isolated duodenum is by increasing intracellular cyclic AMP levels. This may occur by either inhibiting metabolism of the nucleotide or by stimulating its formation. Additionally, many stimulants appear to act indirectly via liberation of endogenous prostaglandins as judged from the marked attenuation of responses in the presence of indomethacin to all agonists apart from exogenous PGE2, forskolin, ICI 63197 (PDE inhibitor), 2-chloroadenosine and diazepam. Whether purinergic agonists and benzodiazepines act directly on the enterocyte or by releasing other paracrine mediators is unknown.
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PMID:Pharmacological profile of duodenal alkaline secretion. 196 81

Changes in the cholinergic, serotonergic, noradrenergic, dopaminergic, GABAergic and somatostatinergic neurons were investigated to determine their roles in Alzheimer's disease (AD). Markers for these systems were analyzed in postmortem brain samples from 20 patients with AD and 14 controls. In the CSF study, markers for the cholinergic neurons (choline esterase, ChE) and for the somatostatinergic neurons (somatostatin-like immunoreactivity, SLI) were assayed for 93 and 75 probable AD patients and 29 and 19 controls, respectively. Activity of choline acetyltransferase (CAT) was decreased by 50-85% in four cortical areas and hippocampus in patients with AD, but not in other areas of the brain, indicating a profound deficit in the function of cholinergic projections ascending from the nucleus basalis to the cerebral cortex and hippocampus in AD. Muscarinic receptor binding was reduced by 18% in the frontal cortex but not in other areas of the brain in AD. Serotonin (5HT) concentrations were reduced (by 21-37%) in hippocampal cortex, hippocampus and striatum; and 5HT metabolite levels were lowered (by 39-54%) in three cortical areas, thalamus and putamen in AD patients. Concentrations of noradrenaline (NA) were reduced (18-36%) in frontal and temporal cortex and putamen. These data imply that serotonergic and noradrenergic projections are also affected in AD but less than the cholinergic neurons. Dopamine (DA) concentrations in AD patients were reduced by 18-27% in temporal and hippocampal cortex and hippocampus, while HVA, the metabolite of DA, was unaltered. Glutamic acid decarboxylase activity was not altered in AD. SLI was decreased (28-42%) in frontal, temporal and parietal cortex, but not in thalamus and putamen in patients with AD. Frontal tangle scores correlated most strongly with cortical CAT activity reduction and less so with decreases of 5HT, NA and DA, indicating a closer correlation with the cholinergic changes and severity of AD than with other neurotransmitter deficiencies. ChE activity and SLI were reduced by 20% and 35%, respectively, in CSF of the whole group of AD patients as compared to the controls. Comparison of CSF findings between four subgroups of dementia severity indicated that the SLI was already reduced in the group of mildest AD (-31%), while ChE activity was not. Although ChE activity in CSF declined in relation to dementia severity, however, the maximal reduction was only modest (-30%). On the other hand, SLI in CSF showed only a slight further reduction (up to -41%) as the dementia become more severe.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurotransmitter changes in Alzheimer's disease: implications to diagnostics and therapy. 198 17

According to "Spleen-Stomach" theory, the effect of Jianpi Yiqi prescription (JPYQ) was observed clinically and studied experimentally. 168 cases manifested as Spleen-Qi ( ) deficiency including chronic gastritis and peptic ulcer (84 cases), chronic glomerulonephritis (44 cases) and vomitus gravidarum-edema of pregnancy (40 cases) were treated with JPYQ. Estimation were made based on their clinical conditions. Serum gastrin, serum cholyglycine, blood acetylcholine and cholinesterase, blood 5-HT and histamine were measured before and after treatment. The overall effective rate was 92.9% in gastritis and peptic ulcer group, 86.3% in nephritis group and 100% in pregnancy group respectively. A marked increase of serum glycocholic acid level was shown in gastritis and peptic ulcer and vomitus gravidarum groups. That was considered as the result of the secretion of cholic acid by this prescription. Clinical improvement was also obtained in nephritis group accompanying disappearance of albuminuria in 36.4%. Blood level of 5-HT and histamine lowered to some extent and tended to be normal. Besides, this prescription markedly inhibited electric stimulated excitement on isolated longitudinal muscle strip of guinea pig's ileum. The mechanism could be the inhibition of release of acetylcholine from Auerbach's plexus by this prescription.
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PMID:[Clinical and experimental study on the prescription of jianpi yipi]. 259 59

In unanaesthetized dogs iv administration of the cholinesterase inhibitor eserine (0.5 mg) induced a clear-cut rise in plasma canine growth hormone (cGH) levels. Diphenhydramine and meclastine, two antagonists of histamine (H) H1 receptors completely suppressed the GH-releasing effect of eserine, while cimetidine, an H2 receptor antagonist, only blunted and delayed it. Two long-lasting serotonin (5-HT) receptor antagonists, metergoline and pizotifen, partially or completely suppressed, respectively, GH release evoked by eserine, whereas fenfluramine, a releaser of neuronal stores of 5-HT and hence a functional activator of 5-HT neurotransmission, was ineffective in this context. Pimozide, a long-acting dopamine receptor antagonist, abolished the effect of eserine, whereas domperidone, which has the same pharmacological properties but does not cross the blood brain barrier, failed to do so. Finally, phentolamine, an antagonist of alpha-adrenoceptors, and propranolol, a beta-adrenergic antagonist, were completely ineffective in preventing the rise in plasma cGH levels induced by eserine, as was naloxone, an antagonist of opiate receptors. All these data demonstrate that, although cholinergic mechanisms are involved in the mechanism(s) underlying cGH release, the final common pathway for GH secretion is not cholinergic. Preservation of dopaminergic and H1 neurotransmission, probably within the blood barrier, is needed to allow the neuroendocrine transduction of cholinergic inputs, whereas the role of 5-HT neurotransmission remains uncertain.
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PMID:Activation of the cholinergic system and growth hormone release in the dog: functional interactions with other neurotransmitters. 298 38

Intrastriatal injection of soman (14.85 nmol) inhibits cholinesterase (ChE) activity in the striatum with much smaller decreases in ChE activity in other brain areas of the rat. As would be expected, there is a substantial increase in striatal acetylcholine (ACh) content shortly after soman injection. However, this increase is no longer significant 1 h following intrastriatal injection. There is no change in striatal KACh 20 min, 1 h or 24 h following soman injection. ACh content is not affected in the parietal cortex, hippocampus, or medulla/pons following intrastriatal soman injection. However, KACh and/or ACh turnover are reduced in these brain areas following soman injection. There is no consistent effect on dopamine (DA) metabolism in any of the brain areas studied. However, serotonin (5-HT) metabolism appears to be affected in the cortex, hippocampus and medulla/pons following intrastriatal injection of soman. Possible mechanisms of the actions of local injection of soman on brain Ach and 5-HT metabolism are discussed, as well as the differences observed between the effects of local and peripheral administration of soman on DA metabolism in the striatum.
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PMID:Effect of intrastriatal injection of soman on acetylcholine, dopamine and serotonin metabolism. 337 62


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