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)

The latex of Euphorbia royleana which has high molluscicidal and anti-cholinesterase activity against Lymnaea acuminata reduced the levels of 5-hydroxytryptamine (5HT) and dopamine (DA) in the nervous tissue of L. acuminata. There was, however, no significant change in the level of 5-hydroxyindole acetic acid (5HIAA). The changes were found to be dependent on concentration of the latex extract. Similar changes were produced by both water and organic solvent extracts of the latex. The latex of E. royleana thus affects all the known neurotransmission mechanisms in the snail either separately or through a complex interaction between the different neurotransmitters. This may account for its high toxicity to snails.
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PMID:Alteration in biogenic amine levels in the snail Lymnaea acuminata by the latex of Euphorbia royleana. 620 25

Characterisation of receptor-mediated breakdown of inositol phospholipids in rat cortical slices has been performed using a direct assay which involves prelabelling with [3H]inositol. When slices were preincubated with [3H]inositol, lithium was found to greatly amplify the capacity of receptor agonists such as carbachol, noradrenaline, and 5-hydroxytryptamine to increase the amount of radioactivity appearing in the inositol phosphates. Using a large variety of agonists and antagonists it could be shown that cholinergic muscarinic, alpha 1-adrenoceptor, and histamine H1 receptors appear to be linked to inositol phospholipid breakdown in cortex. The large responses produced by receptor agonists allowed a clear discrimination between full and partial agonists as well as quantitative analysis of competitive antagonists for each receptor. Whereas carbachol and acetylcholine (in the presence of a cholinesterase inhibitor) were full agonists, oxotremorine and arecoline were only partial agonists. Very low concentrations of atropine shifted the carbachol dose-response curve to the right and allowed inhibition constants for the antagonist to be easily calculated. The nicotinic antagonist, mecamylamine, was ineffective. Noradrenaline adrenaline were full agonists at alpha 1-adrenoceptors, but phenylephrine and probably methoxamine were partial agonists. Prazosin, but not yohimbine, potently and competitively antagonised the noradrenaline inositol phospholipid response. Mepyramine but not cimetidine competitively antagonised the histamine response. These data provide strong confirmation for the potentiating effect of lithium on neurotransmitter inositol phospholipid breakdown and emphasise the ease with which functional responses at a number of cortical receptors can be characterised.
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PMID:Inositol phospholipid hydrolysis in rat cerebral cortical slices: I. Receptor characterisation. 632 32

The stimulatory effect of calcitonin on cerebral acetylcholinesterase activity could not be observed in rats pretreated with p-chlorophenylalanine. The results suggest that the response of the enzyme activity to calcitonin is 5-hydroxytryptamine-mediated.
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PMID:Stimulation of cerebral acetylcholinesterase activity by calcitonin: a possible mediation by 5-hydroxytryptamine. 644 20

Normal megakaryocytes take up and store serotonin (5-hydroxytryptamine) (5-HT). Murine megakaryocyte colonies were grown in plasma clot cultures, labeled autoradiographically with 3H-5-HT-creatinine sulfate, and stained for acetylcholinesterase. Silver granules representing serotonin uptake were present over almost all acetylcholinesterase-positive cells, including both mature megakaryocytes and smaller mononuclear cells. There was no evidence of serotonin accumulation in non-acetylcholinesterase staining granulocytic, monocytic, or erythroid cells. The results of this study provide: (a) a new label to identify murine megakaryocytes and smaller mononuclear megakaryocyte precursors (progeny of CFU-M) in plasma clot cultures, (b) further evidence that immature acetylcholinesterase-positive megakaryocyte precursor cells possess the ability to take up and store serotonin, and (c) evidence that this function of megakaryocytes and megakaryocyte precursors is preserved in the artificial environment of plasma clot cultures.
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PMID:Serotonin uptake by progeny of murine megakaryocyte precursors (CFU-M) in vitro. 648 79

Two groups of male Wistar rats weighing about 140 (WI) and 200 g (WII) and a group of Sprague-Dawley (S.D.) rats (140 g) received oral disulfiram 220-580 mg/kg (DSF) daily for one or three weeks. Isolated ilea of both control and treated rats showed similar responses to acetylcholine, but the responses to 5-hydroxytryptamine (5-HT) were decreased after one and three weeks' treatment in the WI and SD rats. Pretreatment with reserpine intensified this effect in treated WI rats. A distinct decrease in the histochemical reactivity for the acetylcholinesterase and the non-specific cholinesterase was observed in the nerve plexuses of the gut wall indicating a DSF-induced nerve damage. Autonomic (cholinergic) nerves seemed thus to be affected by DSF. The two rats strains studied did not differ in their responses to 5-HT.
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PMID:Neurotoxic effects of disulfiram on autonomic nervous system in rat. 652 6

The effects of multiple intraperitoneal doses of Nuvacron (0.8 mg/kg) or Furadan (0.25 mg/kg) on the concentrations of brain neurotransmitters in mice were studied. The following were measured: acetylcholine, acetylcholinesterase, gamma-aminobutyric acid, epinephrine, norepinephrine, dopamine and 5-hydroxytryptamine. These pesticides caused a significant decrease in acetylcholinesterase activity and a significant increase in acetylcholine, gamma-amino-butyric acid, epinephrine, norepinephrine, dopamine and 5-hydroxy tryptamine concentrations. The increased concentrations of the neurotransmitters in mouse brain might be associated with CNS depressant action induced by the insecticides.
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PMID:Changes of acetylcholine, catecholamines and amino acid in mice brain following treatment with Nuvacron and Furadan. 671 May 41

The inhibition of human erythrocytes and plasma cholinesterase (ChE) by 5-hydroxytryptamine in vitro was studied. Constants characterising this inhibition, namely the inhibition rate for red blood cells RBCs (2.5 x 10(4) (mol/l)-1 min-1) and plasma ChE (1.08 x 10(4) (mol/l)-1 min-1) as well as the rate constant for spontaneous reactivation for RBCs (0.3 min-1) and plasma ChE (0.26 min-1) were calculated. The inhibition of RBCs and plasma ChE by 5-hydroxy-tryptamine was found to be of the competitive type.
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PMID:Inhibition of erythrocyte and plasma cholinesterase by 5-hydroxytryptamine. 689 Aug 35

Endogenous calcitonin was altered in rats by thyroparathyroidectomy, followed by supplementation with thyroxine and calcium. As a result, a reduction in the content of 5-hydroxytryptamine in the brain together with an increase in the concentration of tryptophan in the plasma were observed. The changes were accompanied by a diminution in the activity of both choline acetyltransferase and acetylcholinesterase in the cerebral hemispheres. The results are consistent with those produced by exogenous hormone and suggest that calcitonin probably plays a role in the regulation of 5-hydroxytryptamine levels in the brain.
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PMID:Response of rat brain to calcitonin alteration. 709 70

1. In bovine coronary arteries, cholinesterase staining showed an extensive cholinergic innervation at the adventitia-media junction, and some cholinesterase in the outer but not inner smooth muscle.2. Acetylcholine or methacholine caused large, atropine-sensitive contractions of outer muscle but caused little contraction of inner muscle.3. Fluorescence microscopy for monoamines and for histamine, supported by chemical assays, showed no adrenergic innervation but showed numerous fluorescent cells in the adventitia and the outer 50% of the media which stained as mast cells and contained large amounts of histamine and noradrenaline and some dopamine, but little 5-hydroxytryptamine (5-HT).4. 5-hydroxytryptamine (acting by D receptors) and histamine (acting by H(1) receptors) in high concentrations caused large contractions, of similar size, in inner and outer muscle. In given submaximal concentrations they generally caused more contraction of outer than inner muscle, particularly in the case of histamine, provided that imipramine or desipramine was present to inhibit uptake of the agents by mast cells which were present in the outer part of the artery wall.5. Without blockade of uptake, 5-HT applied to the arteries in submaximal concentrations caused less contraction of outer than inner muscle; histamine still caused significantly more contraction of outer than inner muscle.6. The findings indicate that the cholinergic constrictor nerves of these arteries, unlike adrenergic constrictor nerves of other systemic arteries, act almost solely on outer muscle of the vessel wall; and that mast cells give considerable protection against constriction by 5-HT, but little against histamine, reaching the vessel from its adventitial surface.
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PMID:Constrictor actions of acetylcholine, 5-hydroxytryptamine and histamine on bovine coronary artery inner and outer muscle. 712 Jan 42

In previous investigations, we have demonstrated that cholinesterase inhibitors such as physostigmine (PHY) and heptylphysostigmine (HEP) elicit a significant and simultaneous increase in acetylcholine (ACh) and norepinephrine (NE) levels in the rat cortex. This effect is enhanced by idazoxan, a selective alpha-2 antagonist. These data suggest that a combination of cholinergic and adrenergic drug may improve the pharmacological effect of the cholinesterase inhibitor on cortical neurotransmitters such as ACh-NE. In order to obtain additional information on cortical cortical neurotransmitter interaction, we tested, in the cerebral cortex of the rat, the effect of PHY and HEP in animals pretreated with clonidine (CLO), a selective alpha-2 agonist, on ACh, NE, dopamine and 5-hydroxytryptamine) extracellular levels. We detected no effect of systemic or intracortical CLO administration of ACh levels, but NE, dopamine and 5-hydroxytryptamine levels were all decreased. Systemic coadministration of CLO and PHY significantly elevated ACh levels and decreased NE, dopamine and 5-hydroxytryptamine levels. Systemic coadministration of CLO and HEP produced a significant elevation in ACh levels. Comparison between the two treatment combinations shows that, although CLO coadministration reduces the effect of PHY on ACh levels, HEP administered to animals pretreated with CLO produces a stronger effect than HEP alone. A possible explanation for this difference is the variation in duration of the two drugs on ACh elevation and muscarinic receptor desensitization. As a result of the alpha-2 agonist cholinesterase inhibitor coadministration, our data suggest that such a combination does not represent an advantage as a therapeutical alternative for treatment of cognitive impairment in Alzheimer disease patients.
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PMID:Effects of cholinesterase inhibitors and clonidine coadministration on rat cortex neurotransmitters in vivo. 756 54


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