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)

Enzymes concerned with neurotransmitter metabolism were measured postmortem in 50 regions from the brains of 11 chronic schizophrenics, 2 patients with senile dementia, 1 depressive, and 18 controls. Enzymes studied were tyrosine hydroxylase, dopa decarboxylase, glutamic decarboxylase, choline acetyltransferase (CAT), and acetylcholinesterase. The schizophrenic group had high CAT activities in the hippocampus, caudate, putamen, and nucleus accumbens; the other patients from the same hospital did not. A compensatory response to long- or short-term drug usage is considered, but correlations are hard to establish in the group studied. An alternative hypothesis proposes that the high levels are a compensatory response to defective cholinergic receptors in the affected areas. On this hypothesis, and by analogy with chorea, dopaminergic antagonists would act in schizophrenia by helping to reestablish cholinergic-dopaminergic balance.
Arch Gen Psychiatry 1977 Nov
PMID:Possible changes in striatal and limbic cholinergic systems in schizophrenia. 4 82

Whole blood, plasma, or serum levels of various components were measured in fasting, drug-free control subjects and drug-free schizophrenic patients. Compared to normal controls, chronic schizophrenic patients showed increased alpha2-globulins and decreased plasma cholinesterase activity and ceruloplasmin activity, and acute schizophrenic patients showed decreased alpha2-globulins. Compared to chronic patients, acute schizophrenics showed decreased alpha2-globulins and IgA. Compared to normal controls of similar age, chronic schizophrenic patients weighed less, were shorter, and had smaller body surface area. The acute schizophrenic patients were significantly younger than the normal subjects or chronic schizophrenics but there was no difference in the other physical measurements. The present study indicates no gross disturbances in the blood variables studied. That some differences are statistically significant from controls is of scientific interest, but of no clinical value in the diagnosis of schizophrenia.
Arch Gen Psychiatry 1975 Jun
PMID:Blood protein fraction comparisons of normal and schizophrenic patients. 4 63

We describe prolonged apnea following electrotherapy in a patient who was also being treated with a topical organophosphate anticholinesterase, ecothiophate iodide (phospholine iodide), for glaucoma. The increased duration of action of succinylcholine resulted from low levels of serum cholinesterase that had been caused by the organophosphate. Attention is called to other drugs that directly or indirectly (by lowering serum cholinesterase) interact with succinylcholine chloride resulting in prolonged apnea. Other potential hazards of succinylcholine administration, such as hyperkalemia and cardiac arrhythmias, are also discussed.
Arch Gen Psychiatry 1978 Sep
PMID:Hazards of succinylcholine administration during electrotherapy. 68 74

1. The localization of acetylcholinesterase (AChE) was studied by light and electron microscopy (LM and EM) at the neuromuscular junctions (NMJs) of the abdominal superficial flexor muscle (SFM) and the claw adductor muscle (CAM) of the crayfish in view of reported pharmacological evidence of cholinergic transmission at the former but not at the latter site. 2. Survey of LM with the copper-thiocholine method disclosed staining for AChE, but not for butyrocholinesterase (BuChE), at numerous NMJs of the SFM; neither enzyme was detected at any NMJs of the CAM. 3. With the bis-(thioacetoxy) aurate (I) method, EM examination showed AChE-staining at NMJs of the SFM to be confined to the postjunctional membrane. 4. The published and present findings suggest a unique situation of more than one excitatory transmitter for the skeletal neuromuscular system in the crustacean studied.
Gen Pharmacol 1976 Sep
PMID:Localization of acetylcholinesterase in a crustacean neuromuscular system. 97 38

Acute organophosphate poisoning is known to result in substantial behavioral abnormalities. We assessed psychiatric manifestations of exposure in workers less substantially exposed to organophosphate compounds and showing no obvious signs of toxicity. Commercial pesticide sprayers and farmers recently exposed to organophosphate agents were compared to control subjects on personality tests, a structured interview, and cholinesterase level. The commercial sprayers but not the exposed farmers showed elevated of anxiety and lower plasma cholinesterase than control subjects. Assessment of other behavioral manifestations and red blood cell cholinesterase failed to disclose other group differences. These findings are viewed as tentative until confirmed by additional study, but they point to the possibility that organophosphate compounds may produce subtle defects in workers who are not obviously toxic. The findings do not justify public alarm but do suggest an area warranting more systematic and definitive investigation.
Arch Gen Psychiatry 1976 Feb
PMID:Anxiety associated with exposure to organophosphate compounds. 125 99

The effects of some muscarinic M1 and M2 receptor agonists and antagonists on rat brain serotonergic activity was assessed by noting their effects on the levels of 5-hydroxytryptamine (5-HT) and its major metabolite, 5-hydroxyindole acetic acid (5-HIAA), estimated by a high pressure-liquid chromatographic (HPLC) technique. The muscarinic M1 receptor agonists, arecholine and McN-A-343, and the M2 receptor agonists, gallamine and AF-DX 116, induced a dose-related decrease in the concentrations of both 5-HT and 5-HIAA. On the contrary, scopolamine and the selective M1 receptor antagonist, pirenzepine, increased the levels of the amine and its metabolite. The anti-cholinesterase agent, physostigmine, and the putative M2 receptor agonist, carbachol, induced a dose-related dual effect, with the smaller doses decreasing and the higher doses increasing 5-HT and 5-HIAA concentrations. The results indicate that an inverse relationship exists between the cholinergic and serotonergic neurotransmitter systems in the rat brain due to the likely presence of muscarinic heteroreceptors on serotonergic neurones. The data also indicates that though physostigmine and carbachol may function as M2 receptor agonists, they lose their receptor specificity on dose increment.
J Neural Transm Gen Sect 1992
PMID:Effects of muscarinic receptor agonists and antagonists on rat brain serotonergic activity. 128 83

1. Experiments were designed to determine whether differences exist in the sensitivity to muscarinic and tachykinin agonists in rabbit airways. 2. The rank order of sensitivity (pD2 value) to acetylcholine was: trachea > proximal bronchus > distal bronchus, whereas no regional difference was observed in the sensitivity to carbamylcholine which is resistant to acetylcholinesterase. 3. Acetylcholinesterase activity was greater in the distal than in the proximal airway. 4. In the absence of the peptidase inhibitor, phosphoramidon, the pD2 values of neurokinin A (NKA) and substance P (SP) in trachea were significantly greater than that in bronchus, whereas no regional difference was observed in the NK1 selective agonist, substance P methyl ester (SPOMe). 5. Application of phosphoramidon (10 microM) to avoid peptide degradation abolished the regional difference of the pD2 values of SP. 6. In conclusion, regional differences in sensitivities to acetylcholine and NKA in the rabbit airway were suggested to be due to distribution to the metabolic enzymes of these drugs.
Gen Pharmacol 1992 Nov
PMID:Regional differences of the contractile responses to acetylcholine and neurokinin A in rabbit airway: heterogeneous distribution of the metabolic enzymes. 133 45

1. The novel choline analogs selenonium choline (SeCh) and acetylselenonium choline (ASeCh) have been examined for selected biological activities. 2. ASeCh was found to be an alternative substrate for acetylcholine esterase with Km and Vmax values similar to acetylcholine. 3. ASeCh and SeCh inhibited acetylthiocholine hydrolysis by acetylcholinesterase with IC50 values similar to acetylcholine and choline. 4. SeCh exerted a protective action against physostigmine and DFP induced toxicity. 5. SeCh (85 mg/kg) was found to be 3 times more toxic in mice than choline.
Gen Pharmacol 1992 Jul
PMID:Selected biological activities of novel selenonium choline analogs. 139 75

1. The effect of four hypolipidemic agents with different mechanisms of action (fenofibrate, probucol, colestipol and nicotinic acid) on plasma and liver cholinesterase has been studied. 2. Liver weight and liver weight/body weight ratio increased only after treatment with fenofibrate. 3. Plasma and liver cholinesterase activity increased markedly after fenofibrate, a strong peroxisome proliferator, and slightly after nicotinic acid, a weak peroxisome proliferator. 4. The data obtained suggest that increased cholinesterase activity is due to increased rate of fatty acid oxidation caused by peroxisome proliferators.
Gen Pharmacol 1992 Mar
PMID:Effect of hypolipidemic drugs on cholinesterase activity in the rat. 163 35

Denervated fast-twitch rabbit muscles were progressively losing their fresh weight and the yield of sarcotubular protein was increasing. The activity of Ca(2+)-ATPase was affected but very slightly, the basal Mg(2+)-ATPase and the Mg(2+)-ATPase/Ca(2+)-ATPase ratio however increased together with a simultaneous depression of the membrane-bound acetylcholinesterase activity. We did not observe any differences in density properties of sarcotubular fractions between control and denervated muscle. However, a relative enrichment in SM and H fraction could be seen after denervation with small changes in the content of the Ca(2+)-pump protein, increased levels of calsequestrin and cholesterol, mostly in the heavy and the SM fraction. After denervation the binding sites for 3H-PN-200-110 did not show any changes in receptor affinity, but the number of putative Ca(2+)-channels increased twice along with a depression of 3H-ouabain binding sites. We suggest that the denervation of fast-twitch muscle leads to the hypertrophy of the junctional sarcoplasmic reticulum and the T-system. Changes in the cholesterol content, in the number of putative Ca(2+)-channels and in Na+, K(+)-ATPase can affect the muscle contraction.
Gen Physiol Biophys 1991 Apr
PMID:Effects of denervation on the contents of cholesterol and membrane systems involved in muscle contraction in rabbit fast-twitch sarcotubular system. 165 Jul 29


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