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 this paper a preliminary study was made about the relationship between ACh and the primary input of acupuncture sensation based on the changes of content of ACh, its synthetic enzyme (choline acetylase, or ChAC) and its degradation enzyme (acetylcholinesterase, or AChE) in the dorsal horn of the spinal cord and spinal ganglia. The results were found that: 1) EA at "huantiao" exerted a marked analgesia effect, the acupuncture analgesia was inhibited when the lateral dorsal root was cut off. 2) The content of ACh of the EA group were slightly lower than those of the control group. 3) AChE activity in the spinal ganglia and the dorsal horn increased markedly under electroacupuncture stimulation. 4) The activity of ChAC in the dorsal horn of rats under acupuncture stimulation was significantly higher than those of the control group. 5) ACh content in the spinal ganglia increased obviously when the degradation of peripheral ACh was inhibited by prostigmine. 6) With the lumber dorsal roots excised, AChE activity of the operative side were much lower than those of the intact side during EA stimulation. It suggest that the metabolism of ACh in the dorsal horn of the spinal cord and spinal ganglia change during the course of EAA, and only when signals produced at the acupoints are delivered to the spinal cord via ACh-containing primary somatosensory nerves, can they exert analgesic and therapeutic effect of acupuncture.
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PMID:[The change of ACh metabolism in the dorsal horn of spinal cord and spinal ganglia during electroacupuncture analgesia (EAA)]. 211

In order to investigate the correlation between the peripheral ACh and the primary input of acupuncture sensation, in the paper the cholinesterase inhibitor--Neostigmine and the ACh synthesis blocker--Hemicholine, which are unable to pass through blood brain barrier, and ACh were used as tools to increase or decrease the level of ACh in peripheral nerve system of rats. The results indicated that: 1) The effect of electroacupuncture analgesia can be enhanced by subcutaneous injection of neostigmine which related to the dosage used. 2) The influence of electroacupuncture analgesia can be markedly inhibited by intraperitoneal injection of Hemicholine. 3) This influence of suppression by Hemicholine can be reversed at once when acetylcholine in combination with neostigmine was injected. But could not reverse by neostigmine alone. It suggested that the effect of electroacupuncture analgesia and the primary input of acupuncture sensation were significantly related to the level and content of ACh in periphery.
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PMID:[Acetylcholine and the primary input of acupuncture sensation--influence of peripheral acetylcholine on the role of electroacupuncture analgesia]. 212 63

Two vasoactive intestinal polypeptide (VIP) analogues were observed to induce a concentration-dependent contraction of guinea-pig ileum, which was blocked by atropine but not by tubocurarine. The analogue from guinea-pig, VIP [VIP(gp)], was the most potent inducer of ileum contraction, followed by human-porcine-rat VIP [VIP(hpr)], which differs from VIP(gp) by 4 nonpolar amino acid substitutions. VIP(1-15), composed of only the first 15 of the 28 amino acids of VIP(hpr), was without effect. The relative potency of VIP(gp), VIP(hpr), and acetylcholine was 50 to 100 times more potent in inducing contraction in ileums of which the acetylcholinesterase was inactivated by paraoxon than in the controls. The VIP analogues which induced contraction of ileum also induced secretion of endogenous acetylcholine. The secreted acetylcholine was quantified by high-performance liquid chromatography using electrochemical detection and an immobilized-enzyme column consisting of choline oxidase and acetylcholinesterase. The induction of ileum contraction by VIP(gp), from 10nM to 1 microM VIP, was correlated with the amounts of ACh secreted from ileum. VIP(hpr) induced less acetylcholine secretion than VIP(gp), and was also less potent in causing ileum contraction. VIP(1-15), even at 10 microM, caused neither acetylcholine release nor ileum contraction.
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PMID:Vasoactive intestinal polypeptides induce guinea-pig ileum contraction by causing release of endogenous acetylcholine. 224 24

The effects of acetylcholine (ACh) on the depolarization-evoked release of [3H]gamma-aminobutyric acid ([3H]GABA) have been investigated using synaptosomes prepared from rat corpus striatum and depolarized by superfusion with 9 mM KCl. Acetylcholine inhibited the [3H]GABA overflow in a concentration-dependent manner. The maximal effect was about 50%. The IC50 value (concentration producing half-maximal effect) amounted to 1 microM, in the absence of acetylcholinesterase inhibitors. The effect of ACh on the K(+)-evoked [3H]GABA release was counteracted by the muscarinic receptor antagonist atropine, but not by the nicotinic receptor antagonist mecamylamine or by the selective M1 antagonist pirenzepine. The data show that muscarinic receptors with low affinity for pirenzepine are localized on GABAergic nerve endings in rat corpus striatum where they may directly inhibit the release of GABA.
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PMID:Muscarinic receptors mediate direct inhibition of GABA release from rat striatal nerve terminals. 224 14

1. Possible interactions of contrathion (pralidoxime sulfomethylate), a reactivator of phosphorylated acetylcholinesterase (AChE), with the regulation of cholinergic transmission were investigated on an identified synapse in the buccal ganglion of Aplysia californica. 2. Transmitter release was evoked either by a presynaptic action potential or, under voltage clamp, by a long depolarization of the presynaptic cell. At concentrations higher than 10(-5) M, bath-applied contrathion decreased the amplitude of miniature postsynaptic currents and increased their decay time. At the same time, the quantal release of ACh was transiently facilitated. The facilitatory effect of contrathion was prevented by tubocurarine but not by atropine. Because in this preparation, these drugs block, respectively, the presynaptic nicotinic-like and muscarinic-like receptors involved in positive and negative feedback of ACh release, we proposed that contrathion activates presynaptic nicotinic-like receptors. 3. Differential desensitization of the presynaptic receptors is proposed to explain the transience of the facilitatory action of contrathion on ACh release. 4. The complexity of the synaptic action of contrathion raises the possibility that its therapeutic effects in AChE poisonings are not limited to AChE reactivation.
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PMID:Receptor-mediated presynaptic facilitation of quantal release of acetylcholine induced by pralidoxime in Aplysia. 225 62

The direct measurement of basal and high K(+)-stimulated release of endogenous acetylcholine from striatum and hippocampus slices was achieved without as well as with a cholinesterase inhibitor, physostigmine. Hemicholinium-3, opposite to its well-known activity as an inhibitor of endogenous acetylcholine release, significantly potentiated both the basal and stimulated release, in particular in the absence of physostigmine, suggesting an involvement of some unknown activity stimulating ACh release in hemicholinium-3.
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PMID:Release of endogenous acetylcholine from rat brain slices with or without cholinesterase inhibition and its potentiation by hemicholinium-3. 227 84

1. From denervation studies the trophic influence of the motor nerve on the muscle cell is well documented while little is known about the influence of the muscle on the nerve. Sectioning the axon invariably destroys the nerve terminals and produces nerve degeneration products which themselves may affect nerve and muscle properties. With regard to those difficulties we believe that the botulinal neurotoxins (BoTx) are valuable complements to denervation since they selectively interrupt impulse transmission across the synapse without damaging its morphology. 2. Paralysis of mouse or rat skeletal muscle in vivo with BoTx type A causes marked growth of motor nerve terminals. The sprouting terminals are rich in large dense-core synaptic vesicles containing various neuropeptides and they spontaneously release large quanta of ACh. Thus, it appears that paralysis by BoTx is a strong stimulus for motor nerve growth and the delivery of "trophic" substances to the nerve terminals. 3. Postsynaptically, in extrajunctional areas, paralysis by BoTx induces all the changes observed following denervation, i.e. atrophy, appearance of extra-junctional ACh receptors, TTX-resistant action potentials, a fall of resting membrane potential, fibrillation potentials and the disappearance of extrajunctional acetylcholinesterase activity. Endplate properties are, however, largely maintained. 4. BoTx blockade delays and prevents the retraction of polyneuronal innervation and motoneurone death during development. This supports the suggestion that the paralysed muscle secretes factors essential for growth and for the survival of motoneurones. 5. Like denervated muscle, BoTx paralysed ones, express a high endocytotic activity restricted to a segment in the endplate region.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Trophic interrelations at the neuromuscular junction as revealed by the use of botulinal neurotoxins. 229 Jan 31

2-Deoxy-D-glucose (2-DG) administered intraperitoneally, dose-dependently increased the secretion of gastric acid, and the changes were comparable with those on the activity of choline acetyltransferase (CAT) and acetylcholinesterase (AChE) in the stomach. Double-reciprocal plot analysis of the increased activity of CAT and AChE, induced by 2-DG, showed that the changes were due to the increase of Vmax, with no change in the Km-value for the substrates. The uptake of [3H]choline and subsequent synthesis of [3H]ACh was observed in the forestomach, corpus and antrum of the stomach and in the duodenum. 2-Deoxy-D-glucose significantly increased the uptake of [3H]choline and synthesis of [3H]ACh in every region of the stomach and in the duodenum, in a dose-dependent manner. The increase of secretion of gastric acid, induced by 2-DG paralleled that of uptake of [3H]choline and synthesis of [3H]ACh at an early stage. The conversion of [3H]choline taken up to [3H]ACh was negligibly influenced by 2-DG. Neither the content of ACh and choline, nor the turnover rate of ACh, were changed by administration of 2-DG. 2-Buten-4-olide (2-B4O), which inhibits the activity of the vagus nerve through the central nervous system, prevented 2-DG-induced uptake of [3H]choline and subsequent synthesis of [3H]ACh, as well as the increase in secretion of gastric acid. These results suggest that the uptake of [3H]choline and subsequent synthesis of [3H]ACh are closely related to the neuronal activity of the vagus nerve, and that cholinergic neuronal activity is dependent upon quantitative changes of metabolism of ACh in the gastroduodenum.
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PMID:Alteration of metabolism of acetylcholine induced by 2-deoxy-D-glucose in the gastroduodenum of the rat. 230 15

Immobilized enzyme reactors have been used with high-performance liquid chromatography (HPLC) and electrochemical detection to detect acetylcholine and choline in brain tissue samples. Acetylcholine and choline eluting from the LC column are introduced into a reactor containing immobilized acetylcholinesterase, which hydrolyzes acetylcholine to choline. The product is converted by a second enzyme, choline oxidase, to hydrogen peroxide, which is determined amperometrically. Several novel immobilization techniques including immobilization through enzyme-specific antibodies were used to immobilize these enzymes to retain maximum activity. Improved detection limits were observed when the enzymes were immobilized through the avidin-biotin linkage. Better sensitivity and detection limit were obtained when both enzymes were immobilized together on the same support through the avidin-biotin linkage than when they were separately immobilized and used in two columns. The postcolumn system was applied to brain tissue extracts.
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PMID:Optimization of multienzyme flow reactors for determination of acetylcholine. 231 17

Helical strips of bovine basilar arteries responded to transmural electrical stimulation with moderate relaxations that were abolished by treatment with tetrodotoxin and oxyhemoglobin and were significantly attenuated by quinidine, as were the relaxations previously seen in dog and monkey cerebral arteries. The relaxant response of the bovine arteries was attenuated by treatment with acetylcholine and physostigmine and was significantly potentiated by atropine. In contrast, relaxations of dog coronary arteries to transmural stimulation, mediated via beta-adrenoceptors, were not influenced by physostigmine and atropine but were attenuated by acetylcholine. Abundant fibers containing cholinesterase were histologically demonstrated in bovine basilar arteries, suggesting the presence of cholinergic innervation. Acetylcholine liberated from the cholinergic nerve appears to act on muscarinic receptors located in vasodilator nerve terminals in bovine cerebral arteries and to interfere with the release of vasodilator transmitters.
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PMID:Cholinergic prejunctional inhibition of vasodilator nerve function in bovine basilar arteries. 233 Oct 19


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