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)

Accumulation of acetylcholinesterase (AChE) and choline acetylase (ChAc) activities proximal to a tie placed on the sciatic nerve was measured in control, untreated diabetic, and insulin-treated diabetic rats. In the diabetic animals AChE accumulation was reduced by about 20% and ChAc accumulation by about 40%. Insulin treatment eliminated the impairment. It remains an open question whether these reversible functional changes in rat have any counterpart in the diabetic neuropathy of man.
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PMID:Fast and slow axoplasmic flow in sciatic nerve of diabetic rats. 5 67

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

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 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.
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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.
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PMID:Effect of nomifensine on acetylcholine and choline in the rat striatum and brainstem. 125 20

Synthetic pyrethroid insecticide permethrin significantly decreased the levels of regulatory proteins (S-100 and calmodulin) in the developing CNS of tadpoles of R. cyanophlictis. Remarkable inhibition of enzymes acetylcholinesterase and choline acetylase and significant accumulation of neurotransmitter acetylcholine were observed in permethrin treated animals. Permethrin exposure significantly decreased the activity of phosphodiesterase. The results support molecular disruptions occurring due to permethrin induced toxicity. This in turn may bring about neuronal inefficiency in the treated tadpoles.
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PMID:Insecticide induced disruptions in functioning of developing brain of Rana cyanophlictis. 145 49

In this paper a preliminary study was made about the relationship between ACh and the primary input of acupuncture sensation based on the changes of content of ACh, its synthetic enzyme (choline acetylase, or ChAC) and its degradation enzyme (acetylcholinesterase, or AChE) in the dorsal horn of the spinal cord and spinal ganglia. The results were found that: 1) EA at "huantiao" exerted a marked analgesia effect, the acupuncture analgesia was inhibited when the lateral dorsal root was cut off. 2) The content of ACh of the EA group were slightly lower than those of the control group. 3) AChE activity in the spinal ganglia and the dorsal horn increased markedly under electroacupuncture stimulation. 4) The activity of ChAC in the dorsal horn of rats under acupuncture stimulation was significantly higher than those of the control group. 5) ACh content in the spinal ganglia increased obviously when the degradation of peripheral ACh was inhibited by prostigmine. 6) With the lumber dorsal roots excised, AChE activity of the operative side were much lower than those of the intact side during EA stimulation. It suggest that the metabolism of ACh in the dorsal horn of the spinal cord and spinal ganglia change during the course of EAA, and only when signals produced at the acupoints are delivered to the spinal cord via ACh-containing primary somatosensory nerves, can they exert analgesic and therapeutic effect of acupuncture.
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PMID:[The change of ACh metabolism in the dorsal horn of spinal cord and spinal ganglia during electroacupuncture analgesia (EAA)]. 211

Choline acetyltransferase (Acetyl-CoA:choline O-acetyltransferase, EC 2.3.1.6, abbreviated ChAT), the biosynthetic enzyme for acetylcholine and acetylcholinesterase (EC 3.1.1.7, abbreviated AChE) are expressed in a human cholinergic neuroblastoma cell line, MC-IXC. We have shown that ChAT activity can be regulated in culture by retinoic acid, an active metabolite of vitamin A, and by sodium butyrate, an organic fatty acid. Optimal concentrations of these agents produce 4.3-fold and 1.6-fold increases in ChAT activity, respectively. The effects of retinoic acid are statistically significant after 24 h, whereas for sodium butyrate significant differences are seen only after 48 h. Since retinoic acid stimulation of ChAT activity was reversed only by trypsin treatment and not by removal of retinoic acid from the medium, this suggests that this agent may be acting at the level of the cell surface. Other differentiating conditions, such as culture in serum-free medium or addition of 1-2% dimethylsulfoxide did not increase ChAT activity. Acetylcholinesterase activity was shown to increase only in the presence of sodium butyrate, suggesting that retinoic acid and sodium butyrate may be acting via different pathways. Retinoic acid and sodium butyrate both seem to be permissive rather than instructive in regulating ChAT activity in that they are unable to induce ChAT expression de novo in cell lines which do not already express ChAT activity.
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PMID:Stimulation of choline acetyltransferase activity by retinoic acid and sodium butyrate in a cultured human neuroblastoma. 292 23


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