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)

In male albino rats the electrolytic lesions of the dorsal and median raphe nuclei of the mesencephalon diminished apomorphine-induced aggressiveness (number of attacks, aggressive posture latencies) but didn't influence significantly the intensity of the stereotypy. Both the blockator of tryptophane hydroxylase parachlorophenylamine (PCPA) and 1-tryptophane did not exert any influence on behavioral effects of apomorphine. The raphe-lesion as well as PCPA decreased the level of serotonin and 5-hydroxyindoleacetic acid in the rat forebrain. PCPA decreased in raphe-lesioned rats the dopamine level too. M-cholinoblocking agent atrophine enhanced apomorphine-induced aggressiveness and stereotypy. The blockator of cholinesterase physostigmine had opposite effects. The results suggest that apomorphine induced aggressiveness depends on serotoninergic and cholinergic activity in the brain and there exists a functional link between these neuromediator systems in the CNS.
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PMID:[Analysis of apomorphine aggessiveness and stereotypy: role of serotonin- and cholinergic systems of the brain]. 14 65

We measured cholinesterase (ChE) activity and monoamine metabolite levels in the cerebrospinal fluid (CSF) of 22 patients with early-onset Alzheimer type dementia (Alzheimer's disease; AD) and of 32 controls. Acetylcholinesterase (AChE) activity, 5-hydroxyindoleacetic acid (5-HIAA), and homovanillic acid (HVA) levels were significantly lower in AD patients than in controls. However, there was an overlap in values of each CSF parameter. The measurement of various CSF parameters rather than one alone was more useful as a diagnostic aid. CSF ChE activities correlated with scores on the GBS rating scale, Hasegawa dementia scale, and Wechsler Adult Intelligence Scale, but the monoamine metabolite levels did not. Although cholinergic and monoaminergic deficits may coexist in AD patients, cholinergic deficits tend to be more often associated with cognitive decline than the monoaminergic deficits.
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PMID:Acetylcholinesterase activities and monoamine metabolite levels in the cerebrospinal fluid of patients with Alzheimer's disease. 169 67

The effects of five cholinesterase inhibitors on forebrain monoamine and their metabolite levels, and on forebrain and plasma cholinesterase (ChE) activity in rat were studied in acute and chronic conditions. Acute tetrahydroaminoacridine (THA) dosing caused lower brain (68%) and higher plasma (90%) ChE inhibition than the other drugs studied and increased levels of brain dihydroxyphenylacetic acid (DOPAC) (236%), homovanillic acid (HVA) (197%) and 5-hydroxyindoleacetic acid (5-HIAA) (130%). Acute physostigmine (PHY) administration caused a 215% increase in brain DOPAC content. Despite high brain ChE inhibition induced by metrifonate (MTF), dichlorvos (DDVP) or naled no changes in brain noradrenaline (NA), dopamine (DA) or serotonin (5-HT) occurred due to treatment with the study drugs in the acute study. In the chronic 10-day study THA or PHY caused no substantial ChE inhibition in brain when measured 18 hours after the last dose, whereas MTF induced 74% ChE inhibition. Long-term treatment with THA or MTF caused no changes in monoamine levels, but PHY treatment resulted in slightly increased 5-HT values. These results suggest that MTF, DDVP and naled seem to act solely by cholinergic mechanisms. However, the central neuropharmacological mechanism of action of THA and PHY may involve changes in cholinergic as well as dopaminergic and serotoninergic systems.
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PMID:Effect of acute and chronic cholinesterase inhibition on biogenic amines in rat brain. 171 Nov 62

Diisopropylfluorophosphate (81.5 nmol) was injected directly into the striata of rats to study changes in striatal metabolism of acetylcholine (ACh), 3,4-dihydroxyphenylethylamine (dopamine), and 5-hydroxytryptamine (serotonin) at early time points following acute irreversible inhibition of cholinesterase. Twenty minutes following the intrastriatal injection of diisopropylfluorophosphate, levels of striatal acetylcholine were elevated by 50%, but a decrease in KACh compensated for this change. At 1 h, levels of ACh were still elevated, but not significantly different from control values. However, KACh and, hence, ACh turnover were greatly enhanced at this time. Finally, at 24 h, striatal ACh content was only slightly elevated and KACh and the turnover rate of ACh had returned to control values. Striatal cholinesterase activity remained significantly inhibited at all three times. At none of these times was ACh content or turnover affected in the parietal cortex, hippocampus, hypothalamus, or medulla/pons. Neither dopamine and its metabolites 3,4-dihydroxyphenylacetic acid and homovanillic acid nor serotonin and its metabolite 5-hydroxyindoleacetic acid were significantly affected at any of the three times by intrastriatal diisopropylfluorophosphate treatment. Possible mechanisms of the changes in cholinergic parameters are discussed.
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PMID:Effect of intrastriatal injection of diisopropylfluorophosphate on acetylcholine, dopamine, and serotonin metabolism. 242 Sep 35

Twenty-one patients with acute brain infarction, 8 with transient ischemic attack and 20 controls were investigated for lumbar cerebrospinal fluid (CSF) monoamine metabolites and cholinesterases. The diseased patients were lumbar punctured on 2 occasions, mean Days 1 (0-3) and 5 (3-9) after debut of symptoms. Monoamine concentrations were determined by reverse phase liquid chromatography with electrochemical detection and the cholinergic enzymes were measured photometrically. Increased concentrations of 3-methoxytyramine (3-MT), homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HI-AA) and increased activity of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) in lumbar cerebrospinal fluid was found in patients with acute brain infarction when compared to control values, while the levels of 3-methoxy-4-hydroxyphenylglycol (MHPG) were not altered. No change of any neurotransmitter metabolite concentration/enzyme activity were found between Day 1 and Day 5 in the diseased patients. These data suggest an increased release of these neurotransmitter markers from necrotic brain areas into the cerebrospinal fluid and/or altered barriers between blood, brain and CSF and/or a dysfunction of the arachnoid villi to clear substances from the CSF. We therefore concluded that CSF neurotransmitters may be useful as specific brain markers in acute stroke.
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PMID:Increased monoamine metabolite concentrations and cholinesterase activities in cerebrospinal fluid of patients with acute stroke. 343 5

Spontaneous motor activity and motor coordination were tested in adult female rats after treating with sodium fluoride at 20 or 40 mg/kg dose level daily for 60 days, using an activity chamber and a rota-rod apparatus, respectively. Total protein concentrations were determined in skeletal muscle, liver and serum of similarly treated animals. The activities of total cholinesterase and acetylcholinesterase were determined in blood and brain regions, respectively. Sodium fluoride treatment suppressed spontaneous motor activity. But no change was observed in the motor coordination of these animals. Tissue and serum protein concentrations were decreased. Cholinesterase activity was decreased in the blood and not in brain regions. A failure of sodium fluoride to impair motor coordination indicated that neuromuscular function required for a forced task was not deteriorated in these animals, although skeletal muscles were deprived of protein and blood cholinesterase activity was suppressed. A suppression of spontaneous motor activity suggests that fluoride has, by a central action, inhibited motivation of these animals to exhibit locomotor behavior. A cholinergic mechanism through a change in the activity of acetylcholinesterase may not account for this effect, since sodium fluoride treatment did not alter the activity this enzyme in brain regions. However, an involvement of monoamines may be proposed in view of previously reported finding that excessive fluoride intake has decreased the concentrations of 5-hydroxyindoleacetic acid and increased that of norepinephrine in rat brain.
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PMID:Effects of sodium fluoride on locomotor behavior and a few biochemical parameters in rats. 2178 93