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)

Rats were given bilateral injections of ethylcholine aziridinium ion, AF64A (1 nmol/side) into the basal forebrain (BF). One month later, choline acetyltransferase activity was reduced by 25% in the frontal cortex (FC). There was a marked decrease in cortical uptake of [3H]choline, but [3H]GABA and [3H]dopamine uptake was not affected by the injection. Histological analysis confirmed that this dose of AF64A caused acetylcholinesterase staining in the FC to disappear. Acquisition and retention of a T-maze task were impaired in the rats with BF lesions one month after the injection. Acquisition of the water-filled multiple T-maze task was also impaired by AF64A. These observations suggest that the cholinergic component in the BF is involved in spatial memory.
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PMID:AF64A(ethylcholine aziridinium ion)-induced basal forebrain lesion impairs maze performance. 340 15

Rats were administered the organophosphorus insecticide acephate at 1.0 or 10.0 mg/kg.day for 15 weeks. Blood and brain samples were collected at the end of the treatment and analyzed for cholinesterase, acetylcholinesterase, and glutamic acid decarboxylase activities and catecholamine and amino acid levels. No significant inhibition in the activity of brain AChE was noted at doses of 1.0 or 10.0 mg/kg.day. Low levels of acephate exposure (1.0 mg/kg.day), which did not alter plasma cholinesterase or RBC acetylcholinesterase activity levels, resulted in a significant elevation of plasma epinephrine and norepinephrine levels. Decreased GABA, dopamine, and tyrosine levels and glutamic acid decarboxylase activity were observed in brains of these rats. Similar changes occurred in rats exposed to 10 mg of acephate/kg.day; however, plasma cholinesterase and RBC acetylcholinesterase activities were inhibited. These observations suggest that chronic exposure to acephate altered the activity of the noncholinergic system without altering the cholinergic activity, and that low-level chronic exposure to organophosphorous compounds cannot be predicted by measuring the ChE or AChE enzyme activities.
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PMID:Neurotoxic effects of low-level chronic acephate exposure in rats. 360 37

gamma-Aminobutyric acid (GABA) was applied to the superior cervical ganglion (SCG) of CFY rats in vitro and in vivo, with or without implantation of a hypoglossal nerve, to evaluate the effects of these experimental interventions on the acetylcholine (ACh) system, which mainly serves the synaptic transmission of the preganglionic input. Long-lasting GABA microinfusion into the SCG in vivo apparently resulted in a "functional denervation." This treatment reduced the acetylcholinesterase (AChE; EC 3.1.1.7) activity by 30% (p less than 0.01) and transiently increased the number of nicotinic acetylcholine receptors, but had no significant effect on the choline acetyltransferase (acetyl-coenzyme A:choline-O-acetyltransferase; EC 2.3.1.6) activity, the ACh level, or the number of muscarinic acetylcholine receptors. The relative amounts of the different molecular forms of AChE did not change under these conditions. In vivo GABA application to the SCG with a hypoglossal nerve implanted in the presence of intact preganglionic afferent synapses exerted a significant modulatory effect on the AChE activity and its molecular forms. The "hyperinnervation" of the ganglia led to increases in the AChE activity (to 142.5%, p less than 0.01) and the 16S molecular form (to 200%, p less than 0.01). It is concluded that in vivo GABA microinfusion and GABA treatment in the presence of additional cholinergic synapses has a modulatory effect on the elements of the ACh system in the SCG of CFY rats.
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PMID:Modulation of the acetylcholine system in the superior cervical ganglion of rat: effects of GABA and hypoglossal nerve implantation after in vivo GABA treatment. 398 34

Some enzymatic parameters of neuronal transmission as well as the occurrence and the properties or carboxylic ester hydrolases in the hippocampal region of the wistar rat are investigated by histochemical and comparable biochemical methods. The acetylcholinesterase-, the monoamine oxidase- and the GABA-transaminase reaction are found at fibre structures, the course of which is seen more or less clearly. The histochemical picture of these enzymes is very different in each hippocampal layer and mainly limited by the corresponding number of reacting fibres. The origin and attribution of the fibres to the afferent and efferent systems are discussed. The occurrence of the acetylcholinesterase, the monoamine oxidase and the GABA-transferase as well as of the biogenic amines and the GABA are hints for the existence of cholinergic as well as aminergic and GABA-ergic processes of transmission in the hippocampal region. In the hippocampal region, the cingular and the optic cortex carboxylic ester hydrolases acetylcholinesterase, unspecific cholinesterase and the A-, B- and C-esterase could be demonstrated. The acetylcholinesterase of the hippocampal region is for the most part firmly membrane-bound and exists at least in two multiple, formalin-sensitive forms which are histochemically located in fibre structures. The unspecific cholinesterase, localized in the hippocampal region within vessel and capillary walls, exists in an electrophoretic mobile, formalin-sensitive form. Nearly half of the enzymes is soluble. A preferred binding to definite cell organelles was not demonstrable. In the hippocampal region the 3 multiple forms of the A-esterase are formalin-instable lyoenzymes. Good solubility and high formalin-sensitivity are the reason, why A-esterases are not demonstrable with usually histochemical methods. In the hippo ampal region the B-esterase is tightly bound to n electrophoretic mobile formalin-sensitive form in the microsomal fraction. In the cytoplasm of the neurones the desmoenzyme appears more or less granular. The 3 multiple forms of the C-esterase are formalin-sensitive to a different degree. Good solubility and low formalin-sensitivity, compared to the A-esterases are responsible for the fact, that the C-esterases can be shown histochemically only after en-bloc-fixation. The reaction products are granular. The similar behaviour of C-esterase and acid phosphatase, stated by many tests, suggests the C-esterases of the B- and C-type results in the same reactivity of pyramidal and granular cells of the hippocampal region. Some small, very strongly reacting cells belong to other cell types (probably basket cells or polymorphic cells).
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PMID:[Histochemical and biochemical investigations of the hippocampus and neocortex of the Wistar rat. I. Carboxylic ester hydrolases, transmitter enzymes and transmitters of the normal animal (author's transl)]. 610 39

d-Amphetamine and amitriptyline (AT) were administered daily to female rats from day 7 of pregnancy until birth of the litters. Changes in the concentration of the biogenic amines, some of their metabolites, GABA, and the activities of glutamate decarboxylase, acetylcholinesterase (AChE), and choline acetyltransferase were determined in the whole brain of the offspring. The offspring of the amphetamine-treated rats showed a marked increase in serotonin concentration and that of its metabolite on postnatal day 1. Changes in the concentration of GABA were apparent on days 15 and 21 and were inversely correlated with changes in the activity of the synthesizing enzyme: Choline acetyltransferase and AChE activities were also increased at this time. Changes in neurotransmitter metabolism were not so evident in the offspring of rats treated with AT. The locomotor activity of the 8-, 15-, and 21-day offspring was also assessed. The offspring of the amphetamine-treated rats showed enhanced locomotor activity initially, but the activity decreased relative to the age-matched controls in the 21-day group. Offspring from the AT-treated group showed reduced locomotor activity.
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PMID:The effect of d-amphetamine and amitriptyline administered to pregnant rats on the locomotor activity and neurotransmitters of the offspring. 612 48

Several markers of chick neuroretinal differentiation were monitored in vivo and in culture. All increase markedly between 7 and 20 days of embryonic development in vivo. In vitro, endogenous GABA levels decrease almost immediately, while other neuronal markers increase as in vivo for 2 to 5 days before declining (choline acetyltransferase, acetyl cholinesterase, glutamic acid decarboxylase). Neuronal cell surface markers (binding sites for tetanus toxin, alpha-bungarotoxin, muscimol), however, reach maximal levels only after 8 days in vitro. Glial markers such as carbonic anhydrase and hydrocortisone-induced glutamine synthetase activities are also expressed only transiently in culture.
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PMID:Expression of differentiation markers by chick embryo neuroretinal cells in vivo and in culture. 614 Feb 94

Benzodiazepines (BDZ) interact with specific receptors (R), whose activation improves Cl- -channel gating by the GABA receptor (GABA-R). Neurones, whose GABAergic input has a certain level of activity, will be more inhibited in the presence of BDZ (primary target neurones for BDZ). Secondarily, neurones dependent on the activity of primary target neurones will also be effected. Drugs that interact with GABAergic functions (except the BDZ-R) or with the function of primary or secondary target neurones may inhibit some or all BDZ effects; these are nonspecific BDZ antagonists (e.g. GABA-antagonists, cholinesterase inhibitors, naloxone, methylxanthines). Specific BDZ antagonists inhibit the action of BDZ by blocking competitively the BDZ-R. Ro 15-1788 is the best investigated specific BDZ antagonist. Virtually devoid of any pharmacological action by itself, the compound blocks all typical effects of BDZ. It is well tolerated also in man and will find application in anaesthesiology to shorten the sedative and muscle relaxant effect of BDZ and in emergency services to reverse comatose states after BDZ overdosage. Recently drugs have been found that produce effects opposite to the BDZ tranquilizers by inducing a conformation of the BDZ-R which depresses GABA-mediated Cl- -channel gating. The effects of these inverse agonists (e.g. proconvulsant , convulsant, anxiogenic) are blocked by pure competitive BDZ-R blockers, such as Ro 15-1788.
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PMID:Antagonists of benzodiazepines. 614 9

The release of transmitters was studied in various structures of the basal ganglia in cats implanted with several push-pull cannulas. Local depolarization enhanced Met-enkephalin release in the globus pallidus. Activation of striatonigral substance P(SP) neutrons stimulated the transmitter release from terminals. Unilateral electrical stimulation of the caudate nucleus evoked GABA release in both substantia nigrae and pallidoentopeduncular nuclei. The unilateral facilitation or interruption of nigral SP transmission modified dopamine (DA) release in the ipsilateral caudate nucleus in contrast, modifications of GABAergic or glycinergic nigral transmissions induced bilateral symmetrical effects, whereas bilateral asymmetrical changes in DA release in the two caudate nuclei were seen during the unilateral modification of nigral DA transmission. Changes in the dendritic release of DA induced changes in serotonin release both in the substantia nigra and in the ipsilateral caudate nucleus. Finally, it will be shown that acetylcholinesterase can be released from the substantia nigra and the caudate nucleus through processes dependent on nerve activity.
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PMID:In vivo release of transmitters in the cat basal ganglia. 616 43

The maintenance of differentiated properties and survival rates of enteric neurons, grown in explant cultures for periods of up to 3 weeks, was studied. Using catecholamine fluorescence, immunohistochemistry and autoradiography, it was found that adrenergic neurons, VIP-containing neurons and putative GABAergic neurons, which constitute small subpopulations of guinea pig myenteric neurons in vivo, were all represented in plexus explants after maintenance in culture for 2-3 weeks. The pattern of expression of the transmitter-related enzymes, acetylcholinesterase and monoamine oxidase, paralleled that found in in situ studies. Investigation of neuronal structure by intracellular injection of horseradish peroxidase revealed that the cultured neurons continue to express the wide diversity in gross morphology which characterizes these cells in vivo. Employing autoradiography following uptake of [3H]GABA to label putative GABAergic neurons, their survival rate from days 1 to 15 of culturing was determined. No neuronal death was detected between days 1 and 5, while the number of neurons decreased between days 5 and 15. These observations suggest that enteric neurons maintained in explant cultures survive well and maintain to a high degree their histochemical and morphological properties.
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PMID:The enteric nervous system in tissue culture. III. Studies on neuronal survival and the retention of biochemical and morphological differentiation. 618 11

A previous study identified, by conduction velocity following optic nerve shock, 3 classes of retinal fibers which project to 3 distinct laminae of the goldfish optic tectum. In the present study, the effect of various pharmacological agents on the synaptic efficacy of each of the 3 classes of retinal fibers was assessed by the use of current source-density analysis. All 3 classes of optic fibers appear to be nicotinic cholinergic. Six different nicotinic antagonists were tested. All 6 were effective in decrementing the responses of all 3 classes to a criterion level: alpha-bungarotoxin (10-8 M), alloferin (10-5 M), curare (10-4 M), metocurine (10-4 M), hexamethonium (10-4 M) and gallamine (10-3 M). Atropine, a muscarinic antagonist, had only a slight effect even at 10-3 M. Five nicotinic agonists tested also decremented synaptic responses: nicotine (10-5 M), carbamylcholine (10-4 M), acetylcholine (10-4 M), succinyl choline (10-4 M) and decamethonium (10-3 M), presumably via cellular depolarization and receptor desensitization. Two inhibitors of acetylcholinesterase prolonged the response at 10-4 M and decremented it as well at 10-3 M. Hemicholinium 3, an inhibitor of the high affinity uptake of choline, produced a gradual activity-dependent decrement in the responses. Beta-bungarotoxin, a presynaptically-acting toxin, abolished not only the postsynaptic components but also the presynaptic components at 10-6 M. In all other cases the presynaptic deflections were generally unaffected, and with the exception of the toxins, a return to at least 90% of the control value was achieved. In contrast, GABA (10-3 M) and bicuculine (10-4 M) both produced no discernible effect on the 3 classes of responses, and glutamate (10-3 M) produced only a slight decrement, which probably represents a non-specific effect.
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PMID:Electrophysiologic evidence that retinotectal synaptic transmission in the goldfish is nicotinic cholinergic. 624 64


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