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 effects of lanthanum on the activity of purified preparations of acetylcholinesterase (AChE) from the electric organ of E. electricus and on the activity of AChE in intact electroplaques from the same species were studied. 0.1 mM LaCl3 produced an initial inhibition of purified AChE which was followed by a delayed activation of the enzyme. Upon pretreatment of purified enzyme with LaCl3, initial activity was markedly increased. LaCl3 exerted a marked, concentration-dependent inhibition of intact cell AChE. La3+ and Ca2+ appear to interact competitively. In the presence of both 10 mM CaCl2 and 0.1 mM LaCl3, the initial activitity of purified AChE was increased at lower ACh concentrations and inhibited at ACh concentrations greater than 3 X 10(-4) M. Inhibition of intact cell enzyme by 0.1 mM LaCl3 was relieved by increasing the CaCl2 concentration to 10 mM at ACh concentrations less than 2 X 10(-4) M. The data were analyzed assuming Michaelis-Menten kinetics and interpreted with reference to the differential binding of divalent and trivalent cations to regulatory anionic sites which are separate and distinct from the anionic site of the active center of the enzyme.
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PMID:Interactions of lanthanum with purified and intact cell acetylcholinesterase of Electrophorus electricus. 88 82

Acetylcholine receptors in muscle cells differentiated in vitro were monitored by using 125 I-alpha-bungarotoxin. The number of cholinergic receptors was increased 4-8 fold in 2 days due to inhibition of spontaneous contraction of the muscle fibers. The inhibition of this activity, whether mediated through tetrodotoxin, lidocaine or D-600, did not affect the biochemical differentiation of muscle, as represented by creatine-phosphokinase and acetylcholinesterase activity. "Induction" of receptors by tetrodotoxin was inhibited by cycloheximide, actinomycin-D, or 5-bromotubericidine. Dystrophic muscle responded in vitro to inhibition of contraction similar to normal tissue.
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PMID:Induction of acetylcholine receptors in muscle cultures. 94 69

ACh synthesis and content in the cerebral cortex and brain stem as well as the activity of choline acetylase (AcCh) and acetylcholinesterase (AchE) in brain homogenates were determined after NA administration both in vivo and in in vitro. In in vivo experiments NA was injected intraperitoneally or into the lateral ventricle of the brain. Intraperitoneal injection of NA caused a significant fall of ACh content in the cerebral cortex. AchE activity was inhibited after intraventricular NA injection and in in vitro investigations, in which NA was added into the incubation medium. ACh synthesis and AcCh activity showed no abnormalities after NA administration in vivo and in vitro.
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PMID:Effect of noradrenaline on the content, synthesis and catabolism of acetylcholine in the brain. 94 30

The morphology of motor end-plates in rabbits immunized with Torpedo nicotinic acetylcholine receptor (nAChR) has been studied by light and electron microscopy. Rabbits were studied either after one period of paralysis, some in parallel with electrophysiological recordings of MEPPs and EPPs and of Naja naja alpha-neurotoxin binding properties or after recovery followed by a second paralysis. Changes in the sub-neural apparatus were noted after cholinesterase staining only in the latter group. Ultrastructurally, however, most end-plates in both groups contained a wide range of abnormalities. Many were similar in appearance to those observed in human myasthenia gravis (MG). This further supports the theory that immunized rabbits can be used as a model for myasthenia gravis. In the rabbits with 1 period of paralysis an acute stage of influence on the neuromuscular junction seemed to be present while simplified motor end-plates typical for human MG were mostly found in rabbits with 2 periods of paralysis. Short post-synaptic folds in conjugation with thickeneed membrane-bound vesicles at their tops, inside the basement membrane, were frequently observed. These were interpreted as if the crests of the folds containing nAChR had degenerated and had been budded off. If so, a large number of receptor sites had been lost which would be one possible explanation for the lowered capacity of the muscles to bind Naja naja alpha-neurotoxin. Membrane thickenings with projections and striations were interpreted as reflecting ACh receptors and were observed in the post-junctional membrane without proximity to the nerve terminal. The degeneration of the top of the post-synaptic folds and the occurrence of receptors at other locations within the motor end-plate will result in a widened distance between the nerve terminal and the receptors, which can explain previous interpretations of a presynaptic defect in MG.
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PMID:Morphological observations on motor end-plates in rabbits with experimental myasthenia. 97 17

Rats were treated ip with MAO inhibitos (MAO-I): nialamid (NL), pivalylbenzylhydrazine, tranylcypromine, pheniprazine (Ph) or pargyline, and the leve of total, free and bound acetylcholine (Ach) as well as the acetylcholinesterase (Ach-E) activity were estimated in four parts of rats brain 2 or 16 hr after the treatment. These parameters were estimated also after the treatment with tricyclic antidepressants: desmethylimipramine (DMI), amitriptyline, or protriptiline, and in the conditions of the reversal of reserpine-like syndrom. MAO-I, 2 hr after their application and the reversal of reserpine like-syndrom have not changed the level of measured fractions of Ach in parts of the brain. DMI increased the level of all Ach fractions in the striatum. NL caused the decrease of bound Ach level in all parts of the brain with no changes of free Ach level, 16 hr after the treatment. Ph, 16 hr after the treatment, decrease both fractions of ACh only in the cortex. All studied drugs affected evidently ACh-E activity in various parts of brain. It is concluded that:1) Cholinergic mechanisms in the rat brain are involved in the central action of DMI and of some MAO-I., 3) Cholinergic function of the brain may be modulated by the adrenergic activity, 2) Individual parts of the brain have different susceptibility to the influence of different MAO-I on the ACh-E activity.
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PMID:The influence of antidepressive drugs on the level of acetylcholine and on the acetylcholinesterase activity in the brain of rats. 98 Oct 20

The effect of eight monoquaternary and bisquaternary pyridine aldoxime cholinesterase reactivators was tested on isolated guinea-pig heart atria. 2. Acetylcholine and methylfurthretonium in concentrations ranging from 10(-7) M to 10(-5) M have negative inotropic effects in the electrically stimulated atria and negative chronotropic effects in the spontaneously beating atria. 3. In the presence of higher concentration of cholinesterase reactivators alone, the parameters of heart muscle contractility are significantly altered. 4. Cumulative dose-response curves of methylfurthretonium in the presence of reactivators in the range of concentrations from 10(-5) M to 10(-3) M are shifted parallelly to higher concentrations of the agonist.
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PMID:The effects of some cholinesterase reactivators on contractility of the isolated guinea-pig heart atria. 98 15

1. Rabbit retinas were isolated and superfused with a physiological medium. Ganglion cell activity was recorded during stimulation with focused light, and receptive fields were mapped. Receptive fields were identical to those found in vivo and did not change during a 6-h incubation. After the receptive field of a ganglion cell had been identified, acetylcholine or related agents were introduced singly or in combination into the medium, and their effect on the cell's spontaneous and light-evoked activity was observed. 2. Ganglion cells with on-center or directionally selective receptive fields were excited when ACh was added to the medium. The response to exogenous ACh was prevented by cholinergic antagonists. 3. These cells' spontaneous activity and response to light were enhanced by anticholinesterase and depressed by cholinergic antagonists. Antagonists varied in their ability to block the light-evoked response, with dihydro-beta-erythroidine the most effective. 4. Thresholds for ACh or the related agents were low, ranging from 1 to 40 muM; their effects were rapidly and completely reversed when the retina was returned to control medium. 5. In retinas incubated in medium containing 20 mM Mg2+ and 0.2 mM Ca2+, ganglion cells lost completely both their spontaneous and light-evoked activity, but retained their ability to generate action potentials in response to elevated K+. Ganglion cell activity rapidly returned to normal when the retina was returned to medium containing normal electrolytes. On-center and directionally selective cells were excited by ACh in retinas where synaptic transmission had been inhibited by 20 mM Mg2+ and 0.2 mM Ca2+. 6. The responses of on-center and directionally selective cells to ACh, to anticholinesterase, and to cholinergic antagonists in control medium indicate that the retina contains one or more synapses using ACh as a neurotransmitter. The response to ACh in retinas exposed to 20 mM Mg2+ and 0.2 mM Ca2+ suggests that at least one such synapse in on the ganglion cell itself. 7. Off-center cells were inhomogenous in their response to ACh. Although some responded just as the other classes of cell, the majority responded quite weakly and a subgroup was encountered which was entirely unaffected by even 1 mM ACh, by levels of physostigmine which inactivate virtually all retinal acetyl-cholinesterase, or by high concentrations of cholinergic antagonists. Only 2 of 20 off-cells tested in the presence of 20 mM Mg2+ and 0.2 mM Ca2+ were excited by ACh. Apparently ACh is not a primary transmitter for most off-cells.
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PMID:Responses to acetylcholine of ganglion cells in an isolated mammalian retina. 99 29

We investigated the effects of eserine and ouabain on the permeability of the blood-brain barrier (B.B.B.) as related to the febrile response induced with LPS in rabbit. Results are as follows; The febrile response induced by LPS (0.02 and 1.0 mug/kg) i.v. was suppressed by administration of ouabain (0.06 mg/kg, i.v.). Contrary to the febrile response of LPS given i.c. (10(-4) and 10(-3) mug/kg), the febrile response was not suppressed with the same dose of ouabain. The pyrogenicity of cerebrospinal fluid (CSF) withdrawn at two hours after rabbits had been injected with LPS (25 mug/kg) was suppressed by ouabain (0.06 mg/kg, i.v.). Pyrogenic response was enhanced by pretreatment with eserine (0.5 mg/kg, s.c.) given one hr before LPS (1 mug/kg, i.v.). The pyrogenicity of CSF was also potentiated to a greater extent by pretreatment of eserine than with LPS alone. In the eserinized rabbit (0.5 mg/kg, s.c.), the pyrogenicity of CSF was potentiated to a greater extent by ACh (10 mug/kg, i.v.) than by LPS (1 mug/kg, i.v.) alone. From these data, it is concluded that the inhibition of Na, K-ATPase by ouabain decreases the pyrogenicity of LPS, while the inhibition of cholinesterase by eserine enhances the pyrogenicity.
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PMID:[Effects of eserine and ouabain on the febrile reaction induced by lipopolysaccharide]. 103 14

1. Longitudinal muscle strips of the guinea-pig ileum were incubated in Tyrode solution containing either DFP or physostigmine as cholinesterase inhibitor. After a 90 min preincubation period the acetylcholine resting release into the medium was determined. Acetylcholine was estimated by gas chromatography. 2. The resting release was 0.39 nmol/g times min irrespective of the cholinesterase inhibitor used. In the presence of hexamethonium, or after omission of external calcium, the resting release fell by 50 and 55 per cent, respectively. 3. Oxotremorine (10-5 and 10-4M) significantly inhibited the resting release of acetylcholine by 25 and 33 per cent, respectively. The inhibitory effect of oxotremorine was completely reversed by atropine (3 times 10-7 M). Oxotremorine did not reduce the spontaneous release of acetylcholine that occurred either in the presence of hexamethonium or in the absence of external calcium. 4. The acetylcholine content of the muscle strips was approximately doubled during the preincubation with a cholinesterase inhibitor. The subsequent incubation with oxotremorine did not lead to a further increase in the endogenous acetylcholine content. However, incubation of the muscle strips with oxotremorine in the absence of a cholinesterase inhibitor led to a rise in the endogenous acetycholine concentration. In in vivo experiments, oxotremorine also caused an increase in the acetylcholine content of the muscle strips. The possibility is discussed that the rise in the acetylcholine concentration following the administration of oxotremorine is a consequence of the decreased release. 5. It is concluded that oxotremorine inhibits the resting release of acetylcholine by activation of neuronal muscarinic receptors. The inhibitory effect of exotremorine is linked to that fraction of the acetylcholine resting release that is calcium-dependent and that arises from propagated activity in cholinergic neurones. The results are consistent with the hypothesis of a feed-back control of acetylcholine release mediated by inhibitory muscarinic receptors.
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PMID:Inhibition by oxotremorine of acetylcholine resting release from guinea pig-ileum longitudinal muscle strips. 111 41

1 The observations which Paton (1957) interpreted as 'acute tolerance' and 'dependence' have been confirmed for coaxially stimulated segments of guinea-pig ileum and extended to the contractions evoked by field stimulation in the myenteric plexus-longitudinal muscle preparation. Evidence is adduced that the morphine receptors of the myenteric plexus are not involved in the two phenomena. 2 The contraction of the longitudinal muscle depressed by low concentrations of morphine, or levorphanol, can be restored to control level not only by high concentrations of morphine but also by levorphanol and equally well by its (+)-isomer, dextrorphan, which does not fulfil the stereospecific requirements of the morphine receptor. Acetylcholine output was not increased. 3 When, after restoration of the twitch by high concentrations of morphine, the drug is washed out, contractions become depressed. This effect cannot be due to 'dependence' because either morphine or its antagonist, naloxone, restore the twitch again. 4 In the concentrations used, morphine, levorphanol and dextrorphan inhibit the cholinesterase of homogenates of the myenteric plexus-longitudinal muscle preparation by 10-15%. Since a concentration of physostigmine which causes a similar inhibition also restores the twitch, it is concluded that the described phenomena are best explained by the anticholinesterase effects of the drugs.
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PMID:An analysis of the phenomenon of acute tolerance to morphine in the guinea-pig isolated ileum. 112 85


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