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)

Microwave irradiation of 6 kw at 2450 MHz for 300 msec was sufficient to completely inactivate mouse brain cholinesterase and choline acetyltransferase. After this method of sacrifice, the acetylcholine contents of mouse brain regions, given in nanomoles per gram, were found to be: striatum, 81; medulla-pons, 44; diencephalon-midbrain, 34; hippocampus, 31; cerebral cortex, 26; and cerebellum, 17. Sodium pentobarbital caused a dose-dependent increase in whole brain acetylcholine. A maximal increase of 81% in whole brain was seen at 15 minutes with 80 mg/kg of sodium pentobarbital. The increase in acetylcholine after sodium pentobarbital treatment was not caused by anoxia from respiratory depression or by hypothermia. All brain regions except the cerebellum exhibited an increase in acetylcholine after pentobarbital treatment. Fifteen minutes after treatment, cerebellar acetylcholine was significantly decreased. However, at the time when half of the animals had regained the righting reflex, the unconscious mice showed an increase in cerebellar acetylcholine which was statistically significant as compared to control. The relative accumulation rate of acetylcholine calculated for cerebral cortex and hippocampus was higher than that for striatum although the absolute rate of accumulation of ACh was higher in the striatum. Thus, after sodium pentobarbital treatment, the cerebral cortex and hippocampus exhibit a greater cholinergic response than the striatum.
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PMID:Use of 300-msec microwave irradiation for enzyme inactivation: a study of effects of sodium pentobarbital on acetylcholine concentration in mouse brain regions. 0 94

S.c. injections of cholinergic agents, carbachol, methacholine and bethanechol, into fasted rats caused rapid increases in the plasma concentration of cyclic GMP, with a sharp peak at 5--10 min after the injection. Acetylcholine gave rise to a rapid accumulation of cyclic GMP in plasma only when administered together with physostigmine which produced only a slight, if any, potentiation of the action of the cholinesterase-resistant choline esters. Cyclic AMP also increased after these drugs, but only subsequently to the rise of cyclic GMP; the primary action of the cholinergic drugs appeared to be the increase in cyclic GMP. Atropine was effective not only in abolishing the increase in plasma cyclic GMP induced by cholinergic drugs but also in lowering the baseline level of cyclic GMP. It was concluded that the plasma concentration of cyclic GMP could serve as a good parameter of cholinergic activity in rats.
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PMID:Plasma cyclic GMP: response to cholinergic agents. 2 43

The subsynaptic area of mouse diaphragm fibres was hyperpolarized by 1--2 mV during local curarization of the junctional zone in the presence of the reversible anticholinesteraze prostigmine (6 X 10(-6) M), or after treatment of the muscle with organophosphate cholinesterase inhibitor Soman. In a solution containing 5 mM K+ the mean hyperpolarization was 1.1 +/- 0.27 mV at mean resting potential--70 mV. After adding 2 X 10(-5) M ouabain the hyperpolarization increased to 1.5 +/- 0.25 mV. Removal of potassium ions from the bathing medium also increased curare induced hyperpolarization to 1.80 +/- 0.40 mV. Reactivation of membrane ATP-ase by addition of K+ after a period in K+-free medium reduced the hyperpolarization to zero, where measurements were performed 10--20 min after the readdition. It was concluded that spontaneous non-quantal leakage of acetylcholine occurs at the mouse neuromuscular junction, as it does in the frog (ref. Katz and Miledi 1977). Conditions which block the Na+-K+-dependent ATP-ase of nerve terminals increased the continuous leakage of ACh and activation of the pump decreased it.
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PMID:Electrophysiological examination of transmitter release in non-quantal form in the mouse diaphragm and the activity of membrane ATP-ase. 3 68

The mechanism of neuronal excitation by H+ in the medullary chemosensitive structures was analyzed in brains slices of the rat in vitro. Responses of neurons to H+ in the ventral surface layer were compared with responses to various transmitter substances. Neurons excited by H+ were always also excited by acetylcholine (ACH). ACh increased the activity of 70% of superficial ventral medullary neurons. Effects of noradrenaline and serotonin on the activity of neurons were largely opposite to that of H+. Cholinergic blocking agents like atropine, hexamethonium and mecamylamine depressed the H+-elicited excitation of neurons. The cholinesterase inhibitor, eserine, increased the neuronal activity. In the presence of eserine, a solution of low pH caused further increase in discharge of most neurons. The low pH solution prolonged and augmented the excitatory action of ACh on the ventral medullary neurons. It is concluded that the H+-elicited excitation of neurons in the "chemosensitive" structures is dependent upon intact cholinergic transmission in the surface layer. This may be interpreted as resulting from facilitation and/or prolongation of such a chemical transmission by H+.
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PMID:A cholinergic mechanism involved in the neuronal excitation by H+ in the respiratory chemosensitive structures of the ventral medulla oblongata of rats in vitro. 3 26

In alert monkeys the time course for development of supersensitivity to topical acetylcholine in partially isolated frontal cerebral cortex was determined. Thresholds for paroxysmal discharge fell progressively and markedly during 3 weeks, further in 5 and somewhat more after 6 months. ACh supersensitivity was demonstrated in chronic "isolated" occipital cortex. Epileptiform discharges were recorded selectively from chronic partially isolated frontal cortex on peripheral nerve stimulation and these spread, causing a clinical convulsive siezure when the open end of the isolation extended into the precentral gyrus. The basic mechanisms responsible for the supersensitivity are unknown but evidence presented and much in the pertinent literature is in keeping with the hypothesis that partial isolation of cortical cells, i.e., denervation, deafferentation, or disuse may be important. It is suggrested that peripheral nerve stimulation, like arousal, may cause an outflow of ACh on the normal brain surface and over the open end of a partially isolated area, which, especially, in the presence of a diminished cholinesterase activity (in partially isolated cortex), could act like topical ACh, cause a DC shift and an epileptiform discharge.
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PMID:Time course of development of supersensitivity to topical acetylcholine in partially isolated cortex. 4

The morphological evidence of the primary nerve muscle contacts are described. They consist of areas of cholinesterase activity (detected histochemically) localized on the myotube membranes and of mutiple clusters of ACh receptors whose 125I-alpha-bungarotoxin binding sites are revealed by radio-autography. After the stage of the primary nerve muscle contacts, some of which seem transient, characteristic neuromuscular junctions appear. These neuromuscular junctions which possess subneural infoldings are similar to the end-plates of the Rat in vivo.
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PMID:[Formation of the neuromuscular junction in cultures of rat embryonic cells]. 9 7

The stomach, intestine and uterus were contracted by PGE1. Stimulating effects of ACh and serotonin were augmented in some of these organs, especially in guinea pig uterus. ACh- and serotonin-induced bronchial contraction, however, decreased after administration of PGE1. Bronchial relaxation induced by adrenaline or noradrenaline was unaffected or increased. Antiadrenergic effects were not detected in the organs tested. ACh-induced contractions of frog rectus abdominus was augmented by PGE. The potentiating effect of PGE1 was almost the same in degree as that of physotigmine, although cholinesterase inhibitory effect was not detected in PGE1. Intravenous injection of PGE1 (10 mug/kg) into rabbits caused a relaxation of the intestine, which was contrary to the result with the isolated organ. Administration of PGE1 (1 mug/100 g, i.p. or 0.1, 1 mug/100 g, i.v.) did not show any curative effects on intestinal paralysis in cecectomized rats. The mechasism of action of PGE1 on rat uterus was found to be calcium-dependant.
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PMID:[Effect of prostaglandin E1 on the isolated stomach, small intestine, bronchus and uterus of experimental animals and its intestinal effect in vivo]. 12 77

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

Acetylcholine potentiated the glucose-induced insulin release from microdissected mouse islets of Langerhans but had no effect on basal insulin release. Significant potentiation was obtained with 0.1 micron acetylcholine in the presence of 10 micron eserine and with 1 micron or more acetylcholine in the absence of a choline esterase inhibitor. Carbamylcholine, too, potentiated insulin release. Potentiation was blocked by methylatropine, whereas methylatropine alone had no effect on insulin release. Acetylcholine or carbamylcholine (5-500 micron) had no obvious effect on cyclic GMP or cyclic AMP in the islets. In the presence of 11.1 mM D-glucose, the membrane potential of beta-cells oscillated slowly between a polarized silent state of -50 to -55 mV and a depolarized active state of -33 to -39 mV, at which a fast spike activity occurred. Acetylcholine made the potential stay at the plateau and induced a continuous spike activity pattern. Atropine inhibited the electrical effects of acetylcholine but not those of glucose alone. It is suggested that cholinergic potentiation of insulin release is mediated by changes of transmembrane ionic fluxes, probably without the intervention of cyclic GMP or cyclic AMP.
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PMID:Insulin release, cGMP, cAMP, and membrane potential in acetylcholine-stimulated islets. 21 36

Acetylcholine (25 micromol/l) in the presence of the choline esterase inhibitor physostigmine (67 micromol/l) increased the release of growth hormone and efflux of 45Ca2+ from perifused bovine pituitary slices; the time taken for the maximal response to occur was the same. In batch incubations, acetylcholine (1 micromol/l--1 mmol/l) increased pituitary cyclic GMP concentrations in the pituitary gland within 2 min, and increased incorporation of [3H]inositol and [32P]phosphate into pituitary phosphatidyl inositol within 15 min. Cyclic AMP concentrations were not significantly changed 2 or 5 min after acetylcholine addition. All the tissue responses were inhibited by prior exposure of the tissue to atropine (1 micromol/l) but not by tubocurarine (10 micromol/l--1mmol/l), indicating that the responses were mediated by receptors of the muscarinic type. The similarities between these responses and those to known hypothalamic hypophysiotrophic hormones are discussed.
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PMID:Acetylcholine stimulates growth hormone secretion, phosphatidyl inositol labelling, 45Ca2+ efflux and cyclic GMP accumulation in bovine anterior pituitary glands. 22 Mar 65


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