Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

In a recent study (Skaaring and Bierring, 1976) we found cholinesterase-positive nerve-like structures in the lobules of rat liver, and scanning electron microscopy revealed cords having a distribution pattern similar to that of the cholinesterase-positive structures. To obtain further evidence for an intralobular nerve supply the methods of cobalt and Procion Yellow nerve staining (Stretton and Kravitz, 1968; Iles and Mulloney, 1971; Pitman, Tweedle and Cohen, 1972) were adapted, iontophoretic introduction of the dyes being attempted through cut axonal ends in the surface of small excised blocks of rat liver.
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PMID:Further evidence for the existence of intralobular nerves in the rat liver. 6 29

In rats with cobalt implanted in the right frontal cerebral cortex, acetylcholine (ACh) levels were depressed in the visually non-necotic, surrounding cortex at 7 and 14 days after surgery in comparison with values for controls treated with glass. At 21 days post-implantation, ACh levels were not different for glass and cobalt treatments. Effects of drugs affecting cholinergic function on electro-corticographic (ECoG) epileptiform activity were determined in rats implanted bilaterally with cobalt. The cholinesterase inhibitors, physostigmine and diisopropylfluorophosphate reduced both seizure activity and interictal spiking in these cobalt-treated rats. Hemicholinium-3 (HC-3), given subacutely initially inhibited seizures, but seizure frequency increased later during treatment. HC-3 did not appear to inhibit interictal spiking. These results suggest an involvement of brain cholinergic system in chronic cobalt experimental epilepsy. Seven days after cobalt implantation, HC-3 was less effective in depleting ACh in cerebral cortex adjacent to the cobalt-lesion than in similar tissue from rats with no cobalt implants. This suggests that the cholinergic neurons adjacent to the implant are not highly active at a time when seizure frequency is maximal.
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PMID:Cholinergic involvement in cobalt-induced epilepsy in the rat. 91 28

Following the implantation of cobalt-gelatine pellets into the frontal cortex, epileptiform spikes in both primary and secondary foci developed and reached a peak between 7-12 days post implantation. Histological examination showed a necrotic lesion with terminal and fibre degeneration in brain areas connected with the frontal cortex. Golgi staining at 60 days showed a loss of pyramidal cells in the primary focal area. In the lesion and primary focal areas GABA, glutamate and aspartate were significantly reduced between 5--10 days post implantation. No changes in glutamine and glycine were found in either the lesion or pulmonary focus. No changes in amino acid content were found in the secondary focus or in glass implanted controls at any time. In cobalt-treated rats there were significant reductions in the transmitter related enzymes, glutamate decarboxylase, acetylcholinesterase, choline acetyltransferase and aromatic amino acid decarboxylase in the lesion area and primary and secondary foci at 4--8 days post implantation. Levels of these enzymes had recovered to normal by 24 days. Lactate dehydrogenase was reduced only in the lesion area. Beta-Galactosidase was reduced in the lesion area at 4 days but subsequent rose rapidly paralleling increasing gliosis around the lesion. It is concluded that cobalt-induced epilepsy is associated with relatively selective loss of neuronal tissue and provides a useful model for further investigation relevant to clinical epilepsy.
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PMID:Neurochemical and morphological changes during the development of cobalt-induced epilepsy in the rat. 113 20

This paper reviews chemical models of epilepsy and their relevance in the identification and characterization of anticonvulsants. For each convulsant we discuss possible modes of administration, clinical type(s) of seizures induced, proposed mechanism(s) of epileptogenesis and, where available, responsiveness of the induced seizures to anticonvulsants. The following compounds are reviewed: pentylenetetrazol, bicuculline, penicillin, picrotoxin, beta-carbolines, 3-mercaptopropionic acid, hydrazides, allylglycine; the glycine antagonist strychnine; gamma-hydroxybutyrate; excitatory amino acids (glutamate, aspartate, N-methyl-D-aspartate, quisqualate, kainate, quinolinic acid); monosubstituted guanidino compounds, metals (alumina, cobalt, zinc, iron); neuropeptides (opioid peptides, corticotropin releasing factor, somatostatin, vasopressin); cholinergic agents (acetylcholine, acetylcholinesterase inhibitors, pilocarpine); tetanus toxin; flurothyl; folates; homocysteine and colchicine. Although there are a multitude of chemical models of epilepsy, only a limited number are applied in the routine screening of potential anticonvulsants. Some chemical models have a predictive value with regard to the clinical profile of efficacy of the tested anticonvulsants. Some chemical models may contribute to a better understanding of possible mechanisms of epileptogenesis.
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PMID:Chemical models of epilepsy with some reference to their applicability in the development of anticonvulsants. 139 44

We introduce a one-step histochemical method with cobalt as the precipitating agent for ferrocyanide for the light microscopic demonstration of acetylcholinesterase activity. This method was used to demonstrate acetylcholinesterase in normal cortical fibers and neurons, as well as pathological elements such as plaques and tangles. This procedure can also be easily combined with immunohistochemical methods that use diaminobenzidine as a chromogen.
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PMID:A one-step cobalt-ferrocyanide method for histochemical demonstration of acetylcholinesterase activity in central nervous system tissue. 155 80

The determination of organophosphate and carbamate pesticides was carried out using cobalt phthalocyanine-modified carbon epoxy composite electrodes coupled with acetylcholinesterase or butyrylcholinesterase. Covalent immobilization of enzymes on Immobilon membranes or nylon nets was examined; the highest sensitivity to inhibitors was found for the nylon net containing low enzyme loading and this was subsequently used for the construction of an amperometric biosensor for pesticides. Analyses were done using acetyl- or butyrylthiocholine as substrates; thiocholine produced by hydrolysis in the enzyme membrane was electrochemically oxidized at +300 mV (vs. Ag/AgCl reference). The decrease of substrate steady-state current caused by the addition of pesticide was used for evaluation. With this approach, 1.5 and 8.4 micrograms l-1 of paraoxon and heptenophos, respectively, can be detected in less than 3 min. These detection limits are similar as those obtained when analyses were performed using free cholinesterase and 10 min incubation with inhibitor.
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PMID:Sensitive detection of pesticides using amperometric sensors based on cobalt phthalocyanine-modified composite electrodes and immobilized cholinesterases. 163 47

Acetylcholinesterase (EC 3.1.1.7) activity was demonstrated in whole worm homogenates of adult Ascaridia galli with acetylthiocholine as substrate. The pH optimum was not measurable because of an autohydrolysis of the substrate. The Michaelis constant (Km) was 4 mM with saturation by excess substrate. Optimum enzyme activity was noted at a protein concentration of 200 mg/ml assay medium and at a temperature of 37 degrees C. Arrhenius plot of temperature dependence of the enzyme activity showed an energy of activation (delta Ea) of 28.962 K joule/mole above, and 25.448 K joule/mole below, the transition temperature (37 degrees C). Complete inhibition by eserine (physostigmine), a specific and classical acetylcholinesterase inhibitor, established the identity of the enzyme. A marginally higher enzyme activity was observed in females than in males as well as in homogenates from worms of mixed sexes. The enzyme was markedly activated by divalent metal cations such as Fe2+, Mg2+, Cd2+, Cu2+, Zn2+ and Ca2+, while Co2+ and Mn2+ inhibited the activity. Piperazine adipate at a concentration of 10(-3) M caused 45.5% and albendazole, a benzimidazole anthelmintic, 37.5% inhibition in the enzyme activity, while levamisole and mebendazole proved to be practically ineffective, causing an inhibition of 12 and 9%, respectively.
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PMID:Study of the acetylcholinesterase activity of Ascaridia galli: kinetic properties and the effect of anthelmintics. 178 36

The effects of oxotremorine, arecoline and muscarine on neuromuscular transmission of mouse or rat phrenic nerve-diaphragm were investigated. For some studies of endplate potentials (e.p.p.s) the preparation was immobilized by cutting muscle fibers. Oxotremorine (0.3-10 microM) depolarized endplate membranes, reduced miniature e.p.p. amplitudes but increased frequency, induced spontaneous neural discharges and muscle fasciculations, and produced contracture of denervated mouse diaphragm. In mouse and young rat preparations pretreated with Mn2+, Co2+, Ni2+, Cd2+ or low Ca2+ Tyrode to depress evoked acetylcholine release, oxotremorine 0.3-1 microM increased indirect twitches as well as amplitudes and quantal contents of e.p.p.s. These increases were not observed when the synaptic transmission was not depressed, nor in adult rat preparations. The augmentation by oxotremorine of evoked acetylcholine release persisted in preparations pretreated with neostigmine (1 microM) and tetrodotoxin (20 nM), which inhibited acetylcholinesterase and oxotremorine-induced spontaneous neural discharges. These effects of oxotremorine were mimicked by arecoline but not by muscarine and were antagonized by tubocurarine (0.3 microM) but not by atropine (0.1-10 microM). Atropine alone did not affect indirect twitches, synaptic transmission, tetanic responses evoked by direct stimulation of diaphragms, nor the durations of muscle action potential. The direct twitch responses were only slightly increased by oxotremorine at 2-3 microM. Oxotremorine at high concentrations (greater than 2 microM), depressed indirect twitches and e.p.p. amplitude, and accelerated the run-down of trains of e.p.p.s. The IC50 on indirect twitches was reduced by pretreatment with diltiazem or proadifen, which are known to promote receptor desensitization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nicotinic actions of oxotremorine on murine skeletal muscle. Evidence against muscarinic modulation of acetylcholine release. 207 79

The phototoxicities of six metalloporphyrin dimethylesters (i.e. cobalt (Co), copper (Cu), manganese (Mn), nickel (Ni), tin (Sn) and zinc (Zn) were investigated. Hemolysis of human erythrocytes and inactivation of two enzymes (acetylcholinesterase and beta-galactosidase) were used to assess the phototoxic efficacy of these metal chelates. Tin protoporphyrin (SnPP), the only porphyrin found to hemolyze erythrocytes at a concentration of 40 microM (radiation dose, 230 kJ m-2), was much less efficient than either free protoporphyrin IX or hematoporphyrin. SnPP completely inactivated beta-galactosidase at concentrations above 15 microM (radiation dose, 75 kJ m-2) and drastically interfered with acetylcholinesterase activity at a concentration of 150 microM (radiation dose, 75 kJ m-2). CoPP, CuPP, MnPP, NiPP and ZnPP were ineffective photohemolytic agents at 40 microM (radiation dose, 230 kJ m-2), but inactivated acetylcholinesterase and beta-galactosidase activity to varying degrees. These results suggest that (i) metal ions reduce the phototoxicity of protoporphyrin IX, (ii) different metal ions reduce the phototoxic activity of protoporphyrin IX to different degrees and (iii) the biological activities of the various metal complexes vary in different assay systems.
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PMID:Metalloporphyrin phototoxicity. 212 21

The morphology and projections of neurons in the paraventricular organ (PVO) were studied by means of silver impregnation after intraocular application of cobaltous lysine in the lungfish Protopterus dolloi. Cobalt-labeled neurons were found exclusively in the PVO in the dorsal and infundibular hypothalamus. These bipolar neurons possess one CSF-contacting process that protrudes into the ventricular lumen with a club-shape ending and a thick, ramifying process directed into the hypothalamic neuropil; the ependymofugal processes form intra- and extrahypothalamic projections. Impregnated fibers from paraventricular neurons cross in infundibular and hypothalamic commissures, the commissure of the posterior tuberculum, the postoptic, the habenular, and the anterior commissures. Projections to the infundibulum and the median eminence are relatively sparse; no fibers are labeled in the pituitary gland. Ascending projections to the forebrain are extensive. Major targets include the dorsal hypothalamus, the periventricular preoptic nuclei, the habenula, the subhabenular region, the anterodorsal thalamus, and the medial telencephalic hemisphere (septum). Most ascending fibers follow the medial forebrain bundle; others course in the fasciculus retroflexus and terminate in rostral parts of the ipsilateral habenula. Descending fibers run caudally along the ventral floor of the brainstem. They terminate in the neuropil of the mesencephalic tegmentum, ventral tectum, isthmic region, ventral portions of the reticular formation throughout the rhombencephalon, and extend into the spinal cord. Intraocular application of cobaltous lysine results in selective impregnation of neurons in the PVO and their ascending and descending projections, presumably via uptake of tracer from vascular circulation. These projections do not represent retinofugal or retinopetal projections. We provide conclusive evidence for the existence of a PVO in Protopterus. On the basis of PVO location and acetylcholinesterase histochemistry, we propose subdivisions of the infundibular hypothalamus corresponding to those in amphibians. Ascending PVO projections appear to be particularly well developed in lungfish compared with other species and may be related to specialized endocrine mechanisms in this group of vertebrates.
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PMID:Paraventricular organ of the lungfish Protopterus dolloi: morphology and projections of CSF-contacting neurons. 239 40


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