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

Axonal transport of choline acetyltransferase (ChAc, E.E.:2.3.1.6) and acetyl cholinesterase (AChE, E.C.:3.1.1.7) was studied in the peroneal fascicles of rabbit sciatic nerves. The accumulation of ChAc in the central nerve stump proceeded 5 times more slowly than that of AChE and occurred at a distanct of 2-4 mm proximally from the end, whereas AChE accumulated in the last 2 mm of the stump. In double-ligated segments of the nerve in situ the activity of ChAc decreased at the proximal and increased at the distal end; the activity of AChE rose at both ends, The increase of ChAc activity did not cease until 22 h, whereas that of AChE stopped before 10 h. The intensity of ChAc transport is considerably diminished in the part of axon separated from the nerve cell body. Differences between the behavior of ChAc and AChE are interpreted by the assumption that the axonal transport of ChAc is slow, unidirectional, concerns all of the enzyme in the nerve, and that most of the transported enzyme is not associated with intraaxonal organelles. In contrast to ChAc, the transport of AChE is fast, bidirectional, and concerns a minor proportion of enzyme in the nerve; the transported enzyme is associated with organelles. The rate of proximodistal transport of ChAc is estimated at 4 mm/day (based on the assumption that 100% of the enzyme moves proximo-distally) and that of AChE at 480 mm/day (based on the extimate that 5% of enzyme moved proximo-distally in the present experiments).
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PMID:Transport of choline acetyltransferase and acetylcholinesterase in the central stump and isolated segments of a peripheral nerve. 4 69

1. The axonal transport of acetylcholine (ACh), choline acetyltransferase (ChAc) and cholinesterase (ChE) was estimated in the peroneal nerves of rabbits by measuring the accumulation of each against a nerve crush over a period of 20 hr. 2. Estimates were made of the amounts of these substances that were transported in nerves that had been regenerating for up to 111 days after being crushed or up to 13 days after being cut. 3. The initial response was the same whether the injury was a crush or a cut; the amount of ACh transported was increased, while ChAc and ChE transport was reduced. 4. The amounts of ACh, ChAc and ChE transported tended to return to normal levels when the nerves were allowed to reinnervate the denervated muscles. ChAc transport also showed an early recovery in the cut nerves. 5. The ACh content of the central nerve stump did not alter throughout regeneration but ChAc and ChE contents were reduced at the times when the transport of the enzymes was reduced. 6. These results are discussed in relation to the time course of nerve regeneration.
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PMID:Axonal transport of acetylcholine, choline acetyltransferase and cholinesterase in regenerating peripheral nerve. 8 16

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.
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PMID:The effect of adrenaline on acetylcholine synthesis, choline acetylase and cholinesterase activity. 12 24

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

Neurochemical and psychopharmacological studies of rats were designed to examine four hypotheses which have been proposed to account for the development of behavioral tolerance to the anticholinesterase, diisopropyl fluorophosphate (DFP). The fact that the activity of the enzymes, adenosine triphosphatase, alkaline phosphatase and cytochrome oxidase, did not change concomitantly with behavioral measures during chronic treatment with DFP suggests that nonspecific metabolic changes are unlikely mechanisms of behavioral tolerance. Similarly, a lack of change in choline acetylase activity coupled with constantly high acetylcholine levels (140%) and low cholinesterase activity (28.5%) tends to eliminate end-product inhibition of acetylcholine synthesis as a primary mechanism of tolerance to DFP. Alpha-Methyl-p-tyrosine in doses to 150 mg/kg affected the behaviors of control and DFP-treated rats to a comparable degree, offering no support for the hypothesis that a redundant adrenergic system may replace the cholinergic system during the development of tolerance to DFP. In contrast to these various negative findings, pilocarpine was less effective in suppressing the responding of rats tolerant to DFP than that of control subjects. This confirms other evidence indicating that a decreased sensitivity of cholinergic (muscarinic) receptors is one mechanism underlying the development of tolerance to DFP.
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PMID:Experimental tests of hypotheses about neurochemical mechanisms underlying behavioral tolerance to the anticholinesterase, diisopropyl fluorophosphate. 16 30

Artificial synapses were established in the superior cervical ganglion reinnervated by vagal afferent fibers by heterologous cross-anastomosis between the cranial end of nodose ganglion and the caudal end of superior cervical ganglion in cats. Formation of functional synapses was evidenced by unilateral mydriasis and contraction of the nictitating membrane in response to inflation of the stomach with a balloon or to electrical stimulation of the afferent vagus. Electron microscopic findings indicated that the vagal afferent fibers terminated in the superior cervical ganglion after cross-anastomosis. In the superior cervical ganglion reinnervated by the afferent vagus, activities of choline acetyltransferase and cholinesterase were higher than those in the preganglionically denervated ganglion, but lower than those in the sympathetic preganglionically reinnervated ganglion. Contractions of the nictitating membrane and postganglionic action potentials evoked by electrical stimulation of the vagal artificial preganglionic trunk in the cross-anastomosed ganglion were blocked by treatment with tetraethylammonium and also with atropine. Atropine did not affect these responses in the normal and the preganglionically reinnervated ganglion, except at an early stage after operation. Comparisons of pharmacological properties in normal, anastomosed, preganglionically denervated and reinnervated ganglia indicated that activation of muscarinic receptors in the anastomosed ganglia is probably not secondary to an incomplete nerve supply, but may be dependent on the nature of the nonmyelinated vagal afferent fibers. The possibility that the transmitter involved may be acetylcholine is discussed.
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PMID:Involvement of nicotinic and muscarinic receptors in synaptic transmission in cat superior cervical ganglions reinnervated by vagal primary afferent axons. 20 70

(2-Benzoylethyl)trimethylammonium chloride (BETA), a keto analog of acetylcholine, was synthesized and studied as an inhibitor of human placental choline acetyltransferase (ChA). It is a potent inhibitor of ChA with an 150 of 3.1 X 10(-6) M. The inhibition was rapid in onset and was slowly reversible. Upon dialysis of the inhibited ChA, 50% activity was recovered within about 4.90 hours. BETA was noncompetitive with respect to both substrates of ChA, acetyl-CoA and choline. BETA was selective for inhibiting ChA. It was about 100, and 50, times more potent for inhibiting ChA than acetylcholinesterase, and cholinesterase, respectively. Its activities at muscarinic and nicotinic receptors were negligible at the concentrations where complete inhibition of ChA was obtained. In contrast to the other ChA inhibitors, the styrylpyridines and halogenoacetylcholines, BETA is stable in solution. On prolonged storage (several days at 37 degrees C and pH 7.4), solutions of BETA decomposed partially into trimethylamine and vinylphenylketone. Beta was considerably more stable and more selective than other inhibitors of ChA.
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PMID:(2-Benzoylethyl)trimethylammonium chloride: a new, selective and stable inhibitor of human placental choline acetyl transferase. 30 58

In order to gain insight into the possible role of the ACh-system in the smooth muscle cell, the presence of choline acetyltransferase, acetylcholinesterase and butyrylcholinesterase was studied in the longitudinal muscle of the guinea-pig ileum after the mechanical removal of Auerbach's plexus. Such treatment completely removes all nerve elements as confirmed by histochemistry and electron-microscopic examination. It was found that in the longitudinal muscle devoid of all nervous elements a substantial percentage of the activity of all three enzymes still remained. Ultrastructural localization of acetylcholinesterase and butyrylcholinesterase was observed on the sarcolemma, sarcoplastic reticulum, nuclear membrane and invaginations of the sarcolemma. The localization of cholinesterases coincides with sites which are presumably involved in calcium movements during contraction and relaxation. It is well known that the depolarized smooth muscle responds to exogenous ACh with a reversible, calcium dependent contraction and it was suggested that ACh may act by increasing the influx of calcium through the cell membrane or by liberating calcium from its bound form. The presence of choline acetyltransferase and cholinesterase activities in the muscle cell proper, as well as the localization of cholinesterases on structures connected with calcium movements, support the coexistence of an intrinsic cholinergic mechanism in the smooth muscle.
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PMID:Cholinesterases and choline acetyltransferase in the longitudinal muscle of the guinea pig ileum. 51

Gamma-aminobutyric acid, 0.6, 0.8 and 1.6 mg/rat, ivc, increased the level of acetylcholine (ACh) in the striatum, and in doses 0.2-1.6 mg/rat ivc, accelerated synthesis of ACh. The former effect commenced 5 min. after the injection, reached its peak 15 min. and declined after 30 min. The ACh synthesis increased 15 and 30 min. after the injection and declined after 60 and 120 min. Gamma-aminobutyric acid increased the activity of choline acetyltransferase but did not affect activity of choline esterase.
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PMID:The effect of gamma-aminobutyric acid on the content and metabolism of acetylcholine in the rat striatum. 54 77


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