Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
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.
 ...
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.
 ...
PMID:Experimental tests of hypotheses about neurochemical mechanisms underlying behavioral tolerance to the anticholinesterase, diisopropyl fluorophosphate. 16 30

The effect of reserpine on acetylcholine synthesis, choline acetylase and cholinesterase activity. Acta Physiol. Pol. 1975, 26 (1): 55-61. Reserpine-induced changes in ACh content in various tissues of white rats (cerebral cortex and brain stem, stomach, lungs, heart, spleen) and the effects of reserpine on the synthesis, enzymatic breakdown of ACh, and ChAc activity were studied. Reserpine administered subcutaneously caused a singificant rise in ACh content of the cerebral cortex and insignificant rise in the heart and spleen. Reserpine (in a concentration of 0.25 mug/ml) had no effect on ACh synthesis in vitro. Reserpine in vivo increased significantly ACh synthesis in the brain. No effect of reserpine on ChAc and AChE activity was demonstrated.
 ...
PMID:The effect of reserpine on acetylcholine synthesis, choline acetylase and cholinesterase activity. 113 Feb 19

Nomifensine, at a dose of 40 mg/kg, slightly but significantly increased rat striatal acetylcholine 60 min after i.p. administration without affecting choline levels or choline O-acetyltransferase and cholinesterase activities. This drug had no effect on brainstem acetylcholine. In contrast, d-amphetamine and desipramine both produced a small but significant increase in brainstem acetylcholine. It is suggested that nomifensine increased striatal acetylcholine indirectly through blockade of dopamine uptake.
 ...
PMID:Effect of nomifensine on acetylcholine and choline in the rat striatum and brainstem. 125 20

Redistribution of axonal enzymes as a function of time in vitro was studied in an unbranched segment of frog sciatic nerve. Cholinesterase activity moved peripherally at a rate of 99 mm/day and centrally at 19 mm/day. One-quarter of the total nerve content of the enzyme was estimated to be in motion, one-eighth in each direction. Mitochondrial enzymes (hexokinase and glutamic dehydrogenase) moved peripherally at 20-31 mm/day, centrally at 11-20 mm/day. Only 10% of the total content of these mitochondrial enzymes was in motion. No movement of choline acetylase or 6-phosphogluconic dehydrogenase activity was seen even after 4 days in vitro. However, in a 12 day in vivo experiment choline acetylase moved toward the periphery at a rate of 0.34 mm/day. After a day or so in vitro the distal accumulations of cholinesterase and glutamic dehydrogenase decreased, with a concomitant and quantitatively equivalent increase in enzyme activities at the proximal end of the nerve. It is postulated that during incubation a mechanism for reversing the direction of flow develops in the peripheral stump of the nerve. Vinblastine inhibited central and peripheral flow of both cholinesterase and glutamic dehydrogenase. Movement of cholinesterase was not affected by ouabain, thalidomide, or phenobarbital, nor by K(+) excess (110 mM) or absence.
 ...
PMID:Transport of axonal enzymes in surviving segments of frog sciatic nerve. 411 99

1. Acetylcholine (ACh), cholinesterases and choline acetyltransferase (choline acetylase) were estimated in the neural lobe and hypothalamus of the adult male rabbit. Acetylcholine was also estimated in the neural lobes and hypothalami of some other mammals.2. Acetylcholine-like activity was measured by bio-assay using the leech dorsal muscle preparation.3. Characterization experiments indicated that about 90% of the activity measured was due to acetylcholine.4. Mean acetylcholine content in the neural lobe of the rabbit, after extraction with perchloric acid, was 4.38 +/- 0.98 mug/g fresh tissue, and 4.87 +/- 1.53 mug/g in the hypothalamus.5. Acetylcholine was also found to be present, in comparable concentrations, in the neural lobe of man and in the neural lobes and hypothalami of ox, rat and hedgehog.6. Acetylcholinesterase, present in the neural lobe and hypothalamus of the rabbit, hydrolysed 1.74 +/- 0.11 mu-moles of substrate/min/g and 3.78 +/- 0.60 mu-moles substrate/min/g fresh tissue respectively.7. The concentration of butyrylcholinesterase was about one tenth that of acetylcholinesterase in both tissues.8. Choline acetyltransferase present in the neural lobe and in the hypothalamus synthesized 87 +/- 22 mug ACh/hr/g fresh tissue and 378 +/- 149 mug respectively.
 ...
PMID:Acetylcholine and related enzymes in the neural lobe and anterior hypothalamus of the rabbit. 430 97

Isolated frog sartorii were exposed for 30 minutes to HETP-an irreversible anti-cholinesterase, and were then soaked in Ringer's at 15 degrees C. for 16 hours. At the end of the period of soaking the mean resting potential of the muscle fibers was only 29 mv. The decrease in the resting potential of the HETP-treated muscles was accompanied by a loss of potassium and a gain in sodium by the muscles. The effect of anticholinesterases on sodium extrusion was studied by incubating the muscles in a Ringer's containing half of the normal amount of sodium. The muscles respond by extruding sodium against a concentration gradient into the external medium. Sodium extrusion was blocked by prior exposure of the muscle to HETP, and reversibly blocked by exposure to physostigmine. The inhibition of sodium extrusion by physostigmine was correlated with the inhibition of the intracellular cholinesterase. Sodium extrusion was also blocked by high concentrations of 2-methyl-1,4-napthaquinone 8-sulfonic acid and by alpha-ketoglutarate, which are known to inhibit choline acetylase in vitro. But sodium extrusion was not affected by a third inhibitor of choline acetylase, phenobarbital. Sodium extrusion was unaffected by KCN and partially blocked by IAA. The IAA block was eliminated by the addition of pyruvate. It is concluded that either glycolysis or oxidative metabolism can furnish the energy needed for sodium extrusion.
 ...
PMID:The effect of enzyme inhibitors on the resting potential and on the ion distribution of the sartorius muscle of the frog. 1352 72