Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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. Diabetic modifications of nicotinic receptor-operated noncontractile Ca2- mobilization observed in the presence of anticholinesterase were investigated by measuring Ca(2+)-aequorin luminescence in diaphragm muscles of mice with diabetes induced by injections of streptozotocin (150 mg kg-1, bolus i.v.) and alloxan (85 mg kg-1, bolus i.v.). 2. The diabetic state accelerated the decline of noncontractile Ca2+ transients without affecting their peak amplitude. Insulin treatment reversed this alteration. 3. The increase in contractile Ca2+ transients by cholinesterase inhibition was attenuated 0.6 fold and became resistant to changes in [Ca2+]o in the diabetic state. 4. Changes in extracellular pH from 7.6 to 5.6 depressed the peak amplitude of noncontractile Ca2+ transients without affecting their duration, and enhanced the peak amplitude of contractile Ca2+ transients. 5. These results suggest that the inactivation process of noncontractile Ca2+ mobilization is promoted in diabetic muscles, presumably by desensitization of the nicotinic acetylcholine receptor.
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PMID:Diabetic state-induced rapid inactivation of noncontractile Ca2+ mobilization operated by nicotinic acetylcholine receptor in mouse diaphragm muscle. 859 Sep 90

We have found that non-contractile slow Ca2+ mobilization (RAMIC; Receptor-Activity Modulating Intracellular Ca2+) is generated by motor nerve stimulation with anti-cholinesterase at the skeletal muscle, and desensitizes muscle nicotinic receptor (nAChR). To confirm this Ca2+ mobilization without anti-cholinesterase, acetylcholine (ACh) was locally applied by N2-gas pressure onto endplate region at the mouse phrenic nerve-diaphragm muscle preparation. ACh (0.1-3 mM, 20 microliters) elicited bi-phasic elevation of [Ca2+]i (fast and slow Ca2+ mobilization measured as Ca(2+)-aequorin luminescence) in muscle cells. The peak amplitude of slow Ca2+ mobilization (not accompanied by contraction) was increased by ACh concentration-dependently, whereas that of fast component (accompanied by contraction) reached a maximum response at a lower concentration of ACh. The slow Ca2+ mobilization was blocked by lower concentrations of competitive nAChR antagonists which did not affect the fast Ca2+ transients. Moreover, the slow Ca2+ signal was selectively depressed by a neuronal nAChR antagonist methyllycaconitine. Neither Ca2+ channel blockers nor a Na+ channel blocker tetrodotoxin prevented the generation of the slow Ca2+ mobilization. These results suggest that RAMIC is mobilized through postsynaptic neuronal nAChR subtype to desensitize muscle nAChR at the neuromuscular junction.
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PMID:[Slow Ca2+ (RAMIC) mobilization operated by postsynaptic neuronal nicotinic receptor regulates synaptic function at the mouse neuromuscular junction]. 950 17