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)

Choline acetyltransferase (Ach-T) and acetylcholinesterase (Ach-E) activities in mice brain during the reverse action by imipramine, pheniprazine and pargyline to the syndrome elicited by intraperitoneal administration of Ro 4--1284 were investigated. A single dose of imipramine did not reverse reserpine-like syndrome whereas inhibited Ach-E activity and increased Ach-T activity at the same time. The reversal of reserpine-like syndrome by administration of pargyline, pheniprazine or chronic administration of imipramine was accompanied by no changes in Ach-E and Ach-T activities.
Pol J Pharmacol Pharm
PMID:Choline acetyltransferase and acetylcholinesterase activities in mice brain during the antagonistic action of antidepressant drugs and Ro 4--1284. 2 25

The studies were carried out on mice between the 14th and 19th days, i.e., in the period of maximum penetration of T. spiralis larvae in the host's muscles. Phosphoro-organic esters were given orally to experimental animals in oil solution, at the following doses: Z-50 -- 150 mg per kg of body weight and Z-51 -- 100 mg per kg of body weight. The influence of esters on the activity of cholinesterases was investigated with the Koelle-Friedenwald method, modified by Gomori. The aim of the study was to establish the joint activity of the migrating Trichinella larvae and phosphoro-organic esters on the organism of the host. Z-50 and Z-51 penetrate in therapeutic doses the striated muscles rather weakly. 24 hrs after these compounds were given, acetylcholinesterase (AChE) activity was inhibited in motor end-plates in about 30%, and in muscle fibres infected with T. spiralis larvae in about 60-70%. Pseudocholinesterase (PChE) activity was stronger inhibited than AChE. 24 hrs after applying Z-50 and Z-51 PChE was inhibited in about 90%. Of the two phosphoro-organic esters being examined Z-51 stronger inhibited the cholinesterases activity than Z-50. It was found that the efficiency of phosphoro-organic esters in the course of trichinellosis depends on its ability of infiltration into the host's muscles and on the degree of inhibition of the active cholinesterases in the motor end-plates. Attention was drawn to the fact that increased activity of cholinergic system is one of the main factors in the patholgenesis of the second phase of trichinellosis, i.e., the migration and penetration of the larvae in the muscular fibres of the host.
Pol Arch Weter 1975
PMID:[Histochemical study of the effect of phosphoroorganic esters Z-50 (fenchlorfos) and Z-51 (bromophos) on cholinesteras activity in the course of the muscle phase in experimental trichinellosis in mice]. 5 51

Gastric acid secretion, pepsin concentration in gastric juice and acetylcholinesterase and histidine decarboxylase activities in gastric mucosa of rats treated with dichlorvos (DDVP) were investigated. The increase of HCl secretion, the decrease of acetylcholinesterase activity and enhanced activity of histidine decarboxylase were observed. It is suggested that a higher gastric acid secretion is secondary to histamine production in gastric mucosa, induced by acetylcholine yields gastrin yields histidine decarboxylase mechanism.
Acta Physiol Pol
PMID:Dichlorvos intoxication and gastric secretion. 11 26

The effect of adrenaline on acetylcholine synthesis, choline acetylase and cholinesterase activity. Acta Physiol. Pol. 1975, 26 (1): 45-54. The purpose of the study was to assess the participation of adrenaline in the processes of acetylcholine synthesis and breakdown in white rats. After intraperitoneal administration of adrenaline the content of acetylcholine in the tissues (brain, stomach, sciatic nerve, lumbar spinal cord) initially, slightly decreased, increased in the 30th, 60th, and 120th min, and then fell again below the initial value after 240 min. The rise in acetylcholine tissue content after administration of adrenaline seems to be due to its increased synthesis. This was also confirmed by in vitro investigations. The fall in the tissue acetylcholine content was associated with reduced synthesis of acetylcholine in the cerebral cortex. The increase in acetylcholine synthesis in the brain tissue after adrenaline given in vitro and in vivo does not seem to be caused by activation of choline acetylase. The activity of cholinesterase in the brain was not changed after adrenaline administered in vivo and in vitro.
Acta Physiol Pol
PMID:The effect of adrenaline on acetylcholine synthesis, choline acetylase and cholinesterase activity. 12 24

In Huntington's chorea the biochemical disturbances are to some degree a reverse of those observed in Parkinson's disease and a failure of the cholinergic system is prevalent. Former attempts at treatment were based on blockade of the dopaminergic system. The author suggests that the general line of treatment should be -- similarly as in Parkinson's disease -- not blockade of the predominant system but enhancing the cholinergic activity by administration of acetylcholine precursors and agents blocking cholinesterase. Eight patients were treated in this way and significant improvement was achieved in half of them. Further therapeutic trials along these lines are justified theoretically and the main problem will be to find substances crossing the blood-brain barrier and acting more strongly.
Neurol Neurochir Pol
PMID:[New attempt at treating Huntington's chorea (preliminary report)]. 13 May 61

Hyperkineses are a clinical and pathogenetic counter-part of parkinsonism (MP). Their underlying cause is increased activity of the dopaminergic system or insufficiency of the cholinergic system. Treatment inhibiting the dopaminergic system, similarly as anticholinergic treatment is of little effectiveness in MP. A trial of substitutive treatment was undertaken activating the cholinergic system with a precursor of acetylcholine (dimethyl-amino-ethanol-deanol--Bimanol) with simultaneous inhibition of cholinesterase with prostigmin. The results of this treatment were compared with previously applied antidopaminergic treatment (Haloperidol) and with the effects of L-dopa. This treatment was given to 11 patients with Huntington's chorea (ChH), 4 with faciolingual dyskinesis (DFL), 3 with torticollis spasmodicus (TS), 3 with maladie des tics (MT) and 8 with dyskinesia following treatment with L-dopa (MP). Cholinergizing treatment gave better results than antidopaminergic treatment in TS and ChH, and worse in MT. In dyskinesia following L-dopa cholinergizing treatment gave also no effects reported by others. Differences in the results of cholinergizing and antidopaminergic treatment may indicate non-homogenous pathological mechanism of these hyperkineses. Cholinergizing treatment in hyperkineses is based on a similar principle as L-dopa treatment in MP and this approach seems to be proper but more effective preparations should be sought for.
Neurol Neurochir Pol
PMID:[Cholinergizing treatment in hyperkinesis]. 15 May 48

Adaptation of neuromuscular junction to transmission of impulses after inactivation of acetylcholinesterase. Acta Physiol. Pol., 1977, 28 (1): 23-30. Isolated preparation of rat diaphragm with phrenic nerve was incubated in paraoxon solutions which caused complete inactivation of acetylcholinesterase. This inactivation was associated with disturbances of neuromuscular transmission in the form of blockade of the tetanic response, post-tetanic inhibition of twitch responses and a decreased amplitude of the second response after the first one when two stimuli at a short interval were used. These disturbances were withdrawn somewhat during further incubation of the preparation, although it was kept in paraoxon solution which maintained complete inactivation of acetylcholinesterase. It is suggested that the observed recession of transmission disturbances may be caused by partial adaptation of blockade of the tetanic response, post-tetanic inhibition of twitch blockade of enzymatic hydrolysis of acetylcholine.
Acta Physiol Pol
PMID:Adaptation of neuromuscular junction to transmission of impulses after inactivation of acetylcholinesterase. 19 61

The activity of acetylcholinesterase (AChE 3.1.1.7.) was determined in skeletal muscle homogenates in frogs at various time intervals (15--24 days) after denervation. At the same time changes in AChE activity were compared with morphological changes of neuromuscular end plates in these muscles. Muscle denervation caused initially, within 30 hours, a rise in AChE activity by about 30% in relation to control muscles, followed by its fall to the control values after 4--6 days. The activity decreased further reaching lowest values 15 days after denervation, when it amounted to about 65% of the value of control muscles. After that time, when regeneration of nerves set in, the activity of AChe rose again returning to the control values after 24 hours. In the initial period of denervation no correlation was found between AChE activity and morphological changes in end plates. It was found however in the later period when degenerative changes were most pronounced as well as when reinnervation was in progress.
Acta Physiol Pol
PMID:Effect of skeletal muscle denervaton on the activity of muscular acetylcholinesterase (E.C. 3.1.) in frog. 30 96

Qualitative and semiquantitative histochemical investigations of acetylcholinesterase after a single or repeated administration of isatin, 160 mg/kg ip once or daily for 8 consecutive days have revealed a significant decrease of the histochemical reaction for acetylcholinesterase in chronically treated rats. The cholinergic effect of isatin was tested in the electrophysiological experiment after a single dose of 160 mg/kg isatin and was partially antagonized by atropine.
Pol J Pharmacol Pharm
PMID:Some histochemical and electrophysiological effects of isatin. 52 44

To obtain information about the regulating nervous mechanisms of the pig alimentary canal the activity of monoaminooxidase (MAO) and acetylcholinesterase (AChE) in duodenum, jejunum and colon was studied during the embryonal and postnatal growth. The activity of monoaminooxidase was measured manometrically according to the method prepared by Kolb and that of acetylcholinesterase colorimetrically according to Hestrin's method. It was found that the activity of MAO and AChE in different parts of the pig alimentary canal was considerably differentiated during ontogenesis. Presence of these enzymes was already shown in the embryonal period. However, their activity was poor and almost on the same level in all the examined parts of intestines. Rapid increase of activity of both enzymes was immediately after pigs birth at the time between parturition and fifth day of postnatal life. In the later period of life (6-11 days after birth) there was a decrease of activity of both MAO and AChE only in duodenum. But in jejunum and colon there was a further, slight though, increase of the activity of both enzymes. Comparing the activity of MAO and AChE in the individual parts of the mature pig intestine with the embryonal and postnatal periods, it was found that in spite of the considerable increase of activity of both enzymes after birth, their level was smaller than that in the mature animals.
Pol Arch Weter 1979
PMID:[Monoamine oxidase and acetylcholinesterase activity in the pig's digestive tract in ontogenesis]. 55 10


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