Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following ingestion of [N-14CH3]cocaine (10 mg, 2.3 muCi) by 2 healthy subjects, breath, saliva, serum, and urine samples were collected serially. Labeled CO2 production was monitored as a measure of N-demethylation of cocaine. The cumulative excretion of 14CO2 in 5 hr was 2.4% and 6.2% of the administered dose with half-lives of 2.3 and 1.4 hr, respectively. The greater N-demethylation was found in a subject with lower plasma cholinesterase activity. Radioactivity excreted in 0 to 28 hr urine reached 65% to 75% of the dose. Ecgonine methyl ester, a product of cocaine hydrolysis by plasma cholinesterase, was identified as a major metabolite in the urine of both subjects and accounted for 32% to 49% of the urinary metabolites.
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PMID:Metabolism of cocaine in man. 63 29

The action of the cholinesterase reactivator isonitrosine on gas homeostasis was studied in experiments on intact dogs. It has been found that oxygen consumption and CO2 release by tissues were enhanced within the period from 15 min to 6 days following isonitrosine administration. Simultaneously, oxygen return by the blood was improved. Such action of isonitrosine was unrelated to its effect on the cholinesterase activity of red blood cells.
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PMID:[The effect of isonitrozine on gas homeostasis]. 145 58

14C-carbofuran penetrated readily into seeds of Vicia faba and the rate of penetration was found to be dose dependent. The percentage of bound residues was generally low and did not exceed 3% of the applied dose. When the bound residues were fed to rats 46% of the radioactivity was eliminated via CO2 and urine, while tissues contained 25%. Carbofuran phenol and 3-hydroxy carbofuran represented the main metabolites in the urine. These data indicate that bean-bound carbofuran residues are highly bioavailable to rats. Feeding mice with bound carbofuran residues for 90 days led to inhibition of erythrocyte cholinesterase activity after 30 days (35-40%) while the plasma enzyme remained unaffected. Serum transaminases and blood urea nitrogen were significantly elevated, indicating injury to hepatic and renal structures. The results strongly suggest that the bound residues can induce adverse biological effects in mice.
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PMID:Bioavailability to rats and toxicity in mice of carbofuran residues bound to faba beans. 152 62

The ultrastructural alterations in CA3 pyramidal neurons induced by the irreversible organophosphorus anticholinesterase (OP anti-ChE) pinacolyl methylphosphonofluoridate (soman) and by hypoxia were examined in rat hippocampal slices. During the first 60 min of incubation in control saline, up to 70% of the CA3 pyramidal neurons from slices superfused in control saline showed dilated cisternae of the rough endoplasmic reticulum (ER) or disrupted mitochondria. Fewer cells (10%) displayed heterochromatin clumping. With longer incubations (180 min), the number of cells showing these characteristics declined. During this time, up to 25% of these cells showed indentations in the nuclear envelope. Bath application of saline solutions containing 100 nM soman elicited periodic, spontaneously occurring epileptiform events in the CA3 subfield and substantially reduced (greater than 70%) acetylcholinesterase activity in single slices. The most characteristic ultrastructural alteration observed in response to 100 nM soman (30- to 60-min exposure) was a time-dependent, irreversible increase (up to about 60%) in the number of CA3 pyramidal neurons exhibiting indentations in the nuclear envelope. A morphometric analysis revealed a reversible, soman-induced decrease in the measured nuclear area. To test the hypothesis that these soman-induced alterations were related to hypoxic conditions, the fine structure of CA3 pyramidal neurons was characterized after the control saline was bubbled with nitrogen (95% N2, 5% CO2). In contrast to the effects induced by soman, exposure to nitrogen (15-180 min) caused dilation of rough ER cisternae, created depleted areas within the perikaryon, and produced extensive clumping of heterochromatin. In addition, more CA3 pyramidal neurons showed mitochondrial alterations after exposure to nitrogen than in control or soman-containing saline. Indentations in the nuclear envelope were not observed in response to hypoxia. We concluded that the soman-induced morphological alterations seen in vitro were comparable to those observed in hippocampi from whole animals exposed to sublethal doses of soman. The observations made in this study do not support the hypothesis that the acute alterations induced by soman in the fine structure of CA3 pyramidal neurons were the consequence of hypoxia.
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PMID:Acute ultrastructural alterations induced by soman and hypoxia in rat hippocampal CA3 pyramidal neurons. 339 6

In rabbits anesthetized with 70% N2O-30% O2, the rate of efflux of acetylcholine (ACh) from the cerebral cortex doubled during hypercapnia (increase of end-tidal CO2 from 4 to 8%), and during mild nociceptive stimulation of the tail. Under 0.7% halothane anesthesia, the control rate of ACh efflux was lower than that under N2O; the rate rose 2-fold during hypercapnia and 4-fold during tail stimulation. In the absence of systemic atropinization, increase in ACh efflux was correlated with a shift in EEG from high- to low-voltage ('activated'); after systemic atropinization EEG remained in the high-voltage state, but the changes in ACh efflux with hypercapnia and stimulation were not affected. Following transection of the midbrain, ACh efflux was markedly depressed and did not change during hypercapnia. Taken in context with the previously known facts that the cerebral hyperemia of hypercapnia is potentiated by cholinesterase inhibition and attenuated by atropine or decerebration, the present results support the concept of a cholinergic regulation of the cerebral vasculature.
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PMID:Cortical acetylcholine efflux with hypercapnia and nociceptive stimulation. 402 96

Intraocular grafts of rat hippocampal tissue, grafted either directly from the immature donor brains (fresh) or after storage in liquid nitrogen at -196 degrees C (freeze-stored), were compared with regard to survivability and histological and connective organization. For direct grafting, pieces of hippocampal tissue from rat embryos (embryonic day 19, E21) and newborn rats (PO) were placed in the anterior eye chamber of adult rats immediately after dissection. For grafting after deep-freeze storage, pieces of hippocampal tissue were taken from rat embryos (E16-E21) and newborn rats (PO), frozen at a cooling rate of 1 degrees C/min in CO2 or N2 vapours after addition of the cryoprotective agent dimethylsolfoxide (DMSO), and stored in liquid nitrogen for 1 to 33 days before thawing and intraocular grafting. From 20 to 68 days after grafting, the recipient rats were sacrificed, their eyes sectioned, and the sections stained with thionine for cell bodies, Timm's sulphide silver method for hippocampal fiber systems and terminal fields, and acetylcholinesterase (AChE) for cholinergic fibers and AChE-positive neurons. When examining the 101 grafted eyes (34 grafted with fresh and 67 with freeze-stored tissue) a significantly lower survival rate of the freeze-stored tissue was found (28 vs. 88%). The survivability of the freeze-stored tissue was age-dependent with no survival at donor ages E16 and PO, while tissue from E18-E21 had a 50% survival rate. The grafts of the freeze-stored tissue were also smaller and showed an increased tendency for fragmentation. When evaluating the structure of the grafts, the deep-freeze storage was found primarily to have been harmful to the dentate granule cells and their precursors. The organization of intrinsic fiber connections followed the pattern known from lesion and intracerebral transplant studies. While demonstrating that immature brain tissue can survive deep-freeze storage and subsequent intraocular grafting, the study also indicates that different schemes may have to be used to get optimal survival of different neuronal populations.
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PMID:Intraocular grafts of fresh and freeze-stored rat hippocampal tissue: a comparison of survivability and histological and connective organization. 647 Feb 22

The effects of infusions of ouabain on chemoreceptor activity recorded from the peripheral end of a sectioned carotid sinus nerve were studied in cats anaesthetized with pentobarbitone. Ouabain caused a marked increase in chemoreceptor discharge followed by a decline in discharge to frequencies near or below the pre-ouabain level; during the latter period further administration of ouabain had no effect. Infusion of ouabain during hypoxia further increased the chemoreceptor discharge, but this effect was short-lasting. On intracarotid administration ouabain was less effective in cats with the ganglioglomerular (sympathetic) nerves cut, whereas on intravenous administration no significant difference was observed. Following intravenous administration of ouabain the chemoreceptor peak discharge occurred with dose levels similar to those needed to cause cardiac arrhythmias, but following intracarotid administration the chemoreceptor discharge peaked at doses about 40% of those causing arrhythmias. During ouabain-induced excitation the stimulatory action of NaCN, CO2-equilibrated Locke solution and acetylcholine was potentiated, as was the chemo-inhibition induced by dopamine. During the post-excitatory period the responses evoked by these substances were reduced or abolished. Neither mecamylamine, a nicotinic antagonist, nor physostigmine, an anti-cholinesterase, affected the response of the carotid chemoreceptors to ouabain. The major finding of this study was that ouabain initially 'sensitizes' the carotid body chemoreceptors and then 'desensitizes' them. The most likely mechanism responsible for these effects is the well established Na+--K+-ATPase-inhibiting property of ouabain.
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PMID:Effects of ouabain on carotid body chemoreceptor activity in the cat. 687 75

We report that acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) activities in rat brain were virtually identical whether the rat was anesthetized with carbon dioxide (CO2) before decapitation or decapitated without prior sedation. The AChE and ChAT activities were measured in three brain regions: the hippocampus, cerebral cortex, and cerebellum. Enzyme activities varied significantly by brain region, with the highest values in the hippocampus and the lowest values in the cerebellum. Enzyme activities, however, did not vary with the method of euthanasia, either CO2-induced anesthesia prior to decapitation or decapitation without anesthesia. These data suggest that CO2-induced anesthesia prior to decapitation does not alter activities of these cholinergic markers in rat hippocampus, cerebral cortex, and cerebellum. This method of euthanasia eliminates the need to capture a conscious animal, which reduces stress to the animal and the experimenter.
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PMID:Effects of carbon dioxide-induced anesthesia on cholinergic parameters in rat brain. 798 51

To determine whether local cholinergic mechanisms evoke nitric oxide (NO)-mediated flow-induced vasorelaxation, canine coronary artery rings without endothelium were suspended beneath an organ chamber that contained a stainless steel tube and a femoral artery segment with endothelium. The rings were superfused at a basal rate of 1 ml/min with physiological salt solution that was bubbled with 95% O2-5% CO2 and maintained at 37 degrees C. They were stretched to optimal length and contracted with prostaglandin F 2 alpha (2 x 10(-6) M). When flow through the stainless steel tube (direct superfusion) was increased from the basal rate of 1 to 4 ml/min, coronary force did not change. Superfusion of the rings (n = 8) with effluent from the femoral segment (endothelial superfusion) at 4 ml/min to study flow-induced vasodilation caused a 67.3 +/- 10.8% relaxation. Treatment of the segment with the NO synthase blocker NG-monomethyl-L-arginine (10(-4) M) eliminated the relaxation seen during endothelial superfusion (P < 0.05 vs. control). Application of atropine (10(-6) M) to additional femoral segments (n = 8) abolished the coronary relaxation observed during endothelial superfusion at 1 ml/ min, and the flow-induced relaxation observed at 4 ml/min was reduced from 64 +/- 8.3 to 27 +/- 5.6% (P < 0.05 vs. control). In studies on additional segments and rings (n = 6), the flow-induced relaxations at 4 ml/min of endothelial superfusion were blunted from 86 +/- 10 to 28 +/- 13% after the segments were treated with acetylcholinesterase (0.00028 U/min for 20 min). These data indicate that basal- and flow-induced release of NO from the vascular endothelium can be mediated by local cholinergic mechanisms. It is possible that flow causes acetylcholine release from certain endothelial cells, which stimulates NO release from these cells or from neighboring endothelial cells.
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PMID:Local cholinergic mechanisms mediate nitric oxide-dependent flow-induced vasorelaxation in vitro. 877 18

1. The aim of the present experiments was to characterize the central chemical drive of fictive respiration in the isolated CNS of the newborn opossum, Monodelphis domestica. This opossum preparation, in contrast to those of neonatal rats and mice, produces respiratory rhythm of high frequency in vitro. 2. Fictive respiration was recorded from C3-C5 ventral roots of the isolated CNS of 4- to 14-day-old opossums using suction electrodes. At room temperature (21-23 degrees C) the frequency of respiration was 43 +/- 5.3 min-1 (mean +/- S.E.M., n = 50) in basal medium Eagle's medium (BMEM) equilibrated with 5% CO2-95% O2, pH 7.37-7.40. Respiratory discharges remained regular throughout 8 h experiments and continued for more than 20 h in culture. 3. Superfusion of the brainstem confirmed that solutions of pH 6.3-7.2 increased both the amplitude and frequency of respiration. High pH solutions (7.5-7.7) had the opposite effect and abolished the rhythm at pH 7.7. Addition of ACh (50-100 microM) or carbachol (0.01-10 microM) to the brainstem superfusion also increased the amplitude and frequency of respiratory activity, as did physostigmine (50-100 microM) or neostigmine (20-50 microM). Conversely, scopolamine (50-100 microM) reduced the amplitude and frequency of the basal respiratory rhythm by about 30%. 4. H(+)- and cholinergic-sensitive areas on the surface of the isolated CNS were explored with a small micropipette (outer tip diameter, 100 microns) filled with BMEM (pH 6.5) or 1 microM carbachol. Carbachol applied to H(+)- and cholinergic-sensitive areas in the ventral medulla mimicked the changes of respiratory pattern produced by low pH application. Responses to altered pH and carbachol were abolished by scopolamine (50 microM). Histochemistry demonstrated several medullary groups of neurons stained for acetylcholinesterase. The superficial location of one of these groups coincided with a functional and anatomically well-defined pH- and carbachol-sensitive area placed medial to the hypoglossal roots. 5. Exploration of chemosensitive areas revealed that application of drugs or solutions of different pH to a single well-defined spot could have selective and distinctive effects upon amplitude and frequency of respiratory activity. 6. These results show that fictive respiration in the isolated CNS of the newborn opossum is tonically driven by chemical- and cholinergic-sensitive areas located on the ventral medulla, the activity of which regulates frequency and amplitude of respiration. They suggest that a cholinergic relay, although not essential for rhythm generation, is involved in the central pH chemosensory mechanism, or that cholinergic and chemical inputs converge upon the same input pathway to the respiratory pattern generator.
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PMID:Chemosensory and cholinergic stimulation of fictive respiration in isolated CNS of neonatal opossum. 919 13


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