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)

1. We measured the rate of occurrence of miniature endplate potentials (MEPPs) at identified endplates in frog cutaneous pectoris muscles treated with crude black widow spider venom (BWSV) or purified alpha-latrotoxin (alpha-LTX) in calcium-free solutions, and we examined the relationship between the length of the nerve terminal and the total number of quanta secreted, and the relationship between the number of quanta secreted and the number of vesicles remaining at different times. 2. The venom, or toxin, was applied in a modified Ringer solution with tetrodotoxin, 1 mM-EGTA and no divalent cations, and quantal secretion was started by applying Ca2(+)-free solutions with Mg2+. This was done to synchronize the quantal discharge at the various junctions in a muscle. Ringer solution was applied after the MEPP rate had declined to low levels, and then the muscle fibre was injected with Lucifer Yellow, the endplate stained for acetylcholinesterase and the length of the nerve terminal and the length of a sarcomere were measured on the fluorescent fibre. 3. The total number of quanta secreted by a terminal was measured under a wide variety of experimental conditions: the weights of the frogs ranged from 13 to 68 g, the temperature from 9 to 28 degrees C, and the concentration of Mg2+ from 2 to 10 mM. In one series of experiments the Mg2+ was withdrawn after 3-4 min and reapplied 35-40 min later in order to divide the total output of quanta into two approximately equal bouts of secretion that were well separated in time. 4. The total number of MEPPs recorded at a junction was loosely correlated with the length of its nerve terminal, but it was not affected by the temperature, the concentration of Mg2+ or the division of secretion into well-separated bouts of quantal release. The average total secretion per unit length was about 3700 quanta/sarcomere or about 1200 quanta/microns. 5. The average time course of quantal secretion per micrometre of terminal was determined at single junctions in muscles held at 22-23 degrees C or at 9-10 degrees C. Other muscles were fixed at various times during the course of secretion at each temperature and the number of synaptic vesicles remaining in cross-sections of the terminals were counted on electron micrographs. The number of vesicles remaining per micrometre of terminal was determined from the number per cross-section and the section thickness.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Correlation between quantal secretion and vesicle loss at the frog neuromuscular junction. 212 Apr 25

The effects of soman poisoning on hematological (counts of red blood cells (RBC), white blood cells (WBC), and platelets and measurement of hematocrit) and coagulation parameters (prothrombin time, activated partial thromboplastin time, thrombin time and concentrations of fibrinogen, factor V, factor VII, and factor XI) and serum biochemistry (concentration of albumin, protein, calcium, cholesterol, triglycerides, blood urea nitrogen (BUN), magnesium, and creatinine and activities of alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, cholinesterase, creatinine phosphokinase (CPK), hydroxybutyrate dehydrogenase, and amylase) were determined at 1, 2, 4, 24, and 48 hours after poisoning of rabbits. There were significant (p less than 0.05) decreases in the RBC counts in all treatment groups that were measured initially at 4 hours and were reflected by parallel decreases in the hematocrit values. These changes were probably due to an increase in the hemolysis of the RBC rather than a decrease in the production of RBC. There were minor changes in the coagulation parameters. Generally, the fibrinogen content increased. The activated partial thromboplastin time decreased significantly (p less than 0.05) 24 and 48 hours after soman (50 micrograms/kg) poisoning. Blood cholinesterase values were significantly reduced in all treatment groups at all time periods. The CPK activity was increased after 4 and 24 hours in the 20 and 50 micrograms/kg soman groups. There were minor changes in the other biochemistry values, but none that showed a dose-response relationship; thus, they were considered to be of limited significance with regard to the toxic manifestations of soman exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of soman poisoning on hematology and coagulation parameters and serum biochemistry in rabbits. 212 98

Previous studies with the N18-RE-105 neuronal-like cell line and primary cortical cultures demonstrate that glutamate can produce a calcium-dependent, delayed form of neuronal degeneration that results from its competitive inhibition of cystine transport, which leads to cellular glutathione depletion and death by oxidative stress. Idebenone, a centrally active antioxidant used to treat multiinfarct dementia, protects cells from this form of glutamate-induced cytotoxicity in vitro. In the present study, we have examined the effects of systemic treatment with idebenone on the neurotoxic consequences of intrastriatal injection of kainic acid, quisqualic acid, or quinolinic acid, an NMDA receptor agonist, on neuronal degeneration. Striatal damage was assessed by quantitative neurochemistry with measurement of choline acetyltransferase activity and glutamate decarboxylase activity, by histochemical analysis for acetylcholinesterase and NADPH diaphorase staining and by behavioral assessment of circling produced by systemic apomorphine treatment 10 days after the unilateral lesion. The results indicate that treatment with idebenone provides significant protection against the neuronal degeneration induced by intrastriatal injection of kainic acid and quisqualic acid, but not the NMDA receptor agonist, quinolinic acid. The results suggest that oxidative stress may contribute to the proximate cause of neuronal degeneration induced by quisqualate and by kainate receptor agonists and that the mechanisms of neuronal degeneration caused by quisqualate/kainate receptor agonists differ from those associated with NMDA receptor agonists.
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PMID:Idebenone attenuates neuronal degeneration induced by intrastriatal injection of excitotoxins. 213 66

The biochemical changes of the elements of cholinergic neurotransmission (choline acetyltransferase, ChAT; acetylcholinesterase, AChE; butyrylcholinesterase, BuChE; and muscarinic cholinergic receptors, mAChR) as well as the electrolyte content were studied in ischemic lumbar spinal cord segments of newborn pigs. Ischemia was elicited by ligating the aorta for 30 min. Although no significant changes were observed in the sodium, potassium and calcium content of ischemic spinal cords, the calcium content was slightly elevated, to 119.3% of the control value. Whereas significant depletions were observed in both AChE and ChAT activities (to 69.1 and 87.7% of the control value, respectively), there was no significant change in BuChE activity as compared to the control value. The mAChR were also decreased, from 33.25 +/- 2.2 to 27.18 +/- 1.9 fmol/mg protein, while the Kd value was not significantly altered. It is concluded that even a relatively brief interruption of the oxygen supply can cause severe damage in the lumbar spinal cord of the newborn pig, affecting the cholinergic neurotransmission elements. This animal model might be suitable for studying the effects of hypoxia in newborns and children during chest operations involving the descending aorta.
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PMID:Effects of ischemia on cholinergic neurotransmission and electrolyte content in newborn pig lumbar spinal cord. 215 20

The dihydropyridine calcium channel antagonist nifedipine causes marked reductions in the amounts of acetylcholinesterase (AchE) molecular forms in primary tissue cultures of avian pectoral muscle. These reductions are time-dependent, requiring passage of 3 h prior to any observable response, dose-dependent, with principal actions occurring in the 1-100 nM range, are greater on the 7 S and 19 S forms than on the 11.4 S form, and, based on susceptibility of AchE to irreversible inhibition by a cationic inhibitor, occur almost exclusively with intracellular AchE coincident with a 2-fold reduction in the rate of secretion. The effects are markedly more pronounced in skeletal muscle than in neurons and differ from those observed for verapamil, diltiazem, and the calcium ionophore A23187. These reductions are incompatible with accelerated protein degradation, alterations in posttranslational processing and assembly in the Golgi complex, or enhanced loss of enzyme to the medium, but instead indicate that nifedipine causes a reduction in AchE biosynthesis. Since AchE forms are thought to arise from a single gene, these findings imply a linkage in skeletal muscle between transcription and posttranscriptional processing of mRNA and ligand occupation of the dihydropyridine receptor.
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PMID:Dihydropyridine receptor regulation of acetylcholinesterase biosynthesis. 216 16

Small tissue fragments excised from the electric organ of Torpedo marmorata were treated with diamide, a penetrating thiol oxidizing agent, until synaptic transmission was blocked. At this stage, we found an unexpected number of exo-endocytotic images in the presynaptic plasmalemma. Omega-shaped profiles, some of them coated, were seen in thin sections of fixed tissue and pits opened in the P-face of the presynaptic membrane in freeze-fracture replicas from rapidly-frozen preparations. Diamide-treated specimens were frozen at 1 ms time intervals before, during and after a single electrical stimulus. This stimulation did not result in a further increase in the density of presynaptic pits, not in any change affecting the density or size distribution of intramembrane particles. This result is in contrast with what is observed in untreated specimens where transmission of a nerve impulse is accompanied by a momentary rise in the number of large particles. The density of synaptic vesicles--especially that of a subpopulation of small size vesicles--transiently increased within the first 2 h of diamide treatment. During the first stages of intoxication, diamide prolonged the time course of postsynaptic potentials--both spontaneous and evoked--probably by altering the gating properties of receptors (acetyl-cholinesterase activity was not impaired). Later on, all evoked responses were blocked. The spontaneous transmitter release greatly increased, first in the form of quantal miniature potentials. These then subsided whereas a class of very small potentials was generated at a high frequency. Also under the action of diamide, calcium progressively accumulated in the tissue but the number of synaptic vesicles containing calcium deposits was reduced. It is concluded that diamide causes a marked increase in the number of exo-endocytotic images in the presynaptic membrane, suppresses quantal but not subquantal release, and interferes with calcium sequestration in and extrusion from terminals.
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PMID:Endo-exocytotic images and changes in synaptic transmission induced by diamide at a cholinergic junction. 217 13

The protein and phospholipid composition of microvesicles released from normal human erythrocytes after ATP depletion, on aging or by treatment with merocyanine 540, dimyristoyl phosphatidylcholine or Ca2+/ionophore A23187 has been compared with the composition of the original cell membrane. It has been shown that these microvesicles are depleted of band 3, glycophorin and phosphatidylinositol 4,5-bisphosphate relative to phospholipid by 40% or more. These data are interpreted to mean that less than half of these membrane components are free to diffuse laterally in the lipid bilayer. Acetylcholinesterase was found to be enriched 2-3-fold in microvesicles, possibly because the removal of non-diffusing proteins from the vesiculating region of the lipid bilayer allows more space for freely diffusing proteins like acetylcholinesterase to enter the microvesicle membrane.
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PMID:Restricted diffusion of integral membrane proteins and polyphosphoinositides leads to their depletion in microvesicles released from human erythrocytes. 217 10

The influence of chemical depolarization on the survival and differentiation of acetylcholinesterase (AChE)-containing neurons was examined in primary rat striatal cultures, maintained in different types of media (serum-free and serum-supplemented) and substrate (poly-ornithine and astrocyte monolayer). Chronic application of 5 microM veratridine resulted in a significant loss of neurites by AChE-positive cells, while a higher concentration (20 microM) reduced the number of stained cell bodies. These effects appeared to be selective with regard to AChE-positive cells, as indicated by morphological observations of the cells in the treated cultures and receptor binding measurements. Similarly, elevation of extracellular KCl levels (20-60 mM) produced a dose-dependent neurite loss by AChE-containing cells. Blockers of voltage-sensitive Ca2+ channels--verapamil (1 microM) and nifedipine (1 microM)--did not affect the veratridine-induced neurite loss, while tetrodotoxin (0.1 microM) had a partial effect. When cultures treated with 5 microM veratridine were allowed to recuperate for several days, the number of AChE-positive cells possessing neurites returned close to control values, thus indicating the reversibility of the effect of chemical depolarization. The possibility that chronic neuronal depolarization in the striatum might play a role in regulation of the neuronal processes outgrowth by AChE-containing cells is discussed.
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PMID:Factors regulating the expression of acetylcholinesterase-containing neurons in striatal cultures: effects of chemical depolarization. 217 31

Intracellular Ca2+ mobilization in neuro-skeletal muscle synapse was studied by measuring Ca2(+)-aequorin luminescence transients (Ca2+ transients). Ca2+ transients were categorized into three groups as follows: (1) The 1st phase of rapid Ca2+ mobilization was accompanied with twitch tension, (2) the 2nd phase of slow Ca2+ mobilization was not accompanied with twitch tension, and only observed in the presence of cholinesterase inhibitors, and (3) the 3rd phase was spontaneous Ca2+ mobilization which was rather related to contracture. The caffeine effects were composed of 1st phase-potentiation (cyclic AMP increase?), 2nd phase-inhibition (n-acetylcholine receptor (AChR) closely related), and the increase of 3rd phase (Ca2+ release from salcoplasmic reticulum). d-Tubocurarine showed much higher potency for the inhibition of the 2nd phase than for that of the 1st phase. These results suggest that the 1st phase Ca2+ transients are related to T-type n-AChR channel, whereas the 2nd phase Ca2+ transients are related to S-type n-AChR channel and its mediated signal transduction.
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PMID:[Intracellular calcium ion mobilization and nicotinic acetylcholine receptor-mediated signal transduction in neuro-skeletal muscle synapse]. 219 1

1. Differentiation of excitable cells was studied electrophysiologically and histochemically in cleavage-arrested blastomeres isolated from early ascidian embryos. Blastomeres were isolated at the 4- or 8-cell stage, and cultured in sea water containing cytochalasin B until the time of hatching of control larvae. Electrical responses, immunoreactivity to epidermis-specific monoclonal antibody (2C5) and activity of muscle-specific acetylcholinesterase were examined. 2. All cleavage-arrested blastomeres isolated from an 8-cell embryo differentiated to elicit either muscular- or epidermal-type action potentials, but no neural-type action potentials were observed in these blastomeres. The anterior-animal and the posterior-animal blastomeres developed only epidermal-type action potentials, which involved expression of Ca2+ channels and immunoreactivity to 2C5. One-third of anterior-vegetal blastomeres developed epidermal-type action potentials which are mediated by Ca2+ channels though the immunoreactivity to 2C5 was absent. A majority of remaining blastomeres showed action potentials composed of Ca2+ currents and TEA-sensitive delayed K+ currents (type I response), and a few of them had fast transient K+ currents (A-currents) in addition (type II response). One-third of posterior-vegetal blastomeres developed epidermal-type action potentials without expression of the immunoreactivity to 2C5. The remainder differentiated into muscular-type cells, which expressed Ca2+ currents, TEA-sensitive and TEA-insensitive delayed K+ currents, and showed acetylcholinesterase activity. 3. Cleavage-arrested blastomeres isolated from a 4-cell embryo also differentiated into epidermal- or muscular-type cells, but not neural-type cells. The anterior blastomere, which is the parent cell of anterior-animal and anterior-vegetal blastomeres of an 8-cell embryo, developed epidermal-type, type I or type II responses, as was the case in the anterior-vegetal blastomere isolated from an 8-cell embryo. The posterior blastomere, which was the parent cell of posterior-animal and posterior-vegetal blastomeres of an 8-cell embryo, differentiated into either epidermal-type or muscular-type cells in terms of both membrane excitability and immunochemical reactivity. 4. Cleavage-arrested 1-cell embryos differentiated exclusively into epidermal-type cells in terms of membrane excitability and 2C5 immunoreactivity, even when the cytochalasin B concentration was decreased below 0.1 microgram/ml.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Differentiation of membrane excitability in isolated cleavage-arrested blastomeres from early ascidian embryos. 221 8


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