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)

The effect of 4-aminopyridine, a potassium channel blocker on the muscarinic and opiate modulation of acetylcholine release, was investigated. Rat frontal cortical slices were loaded with [3H]choline, superfused continuously, and stimulated electrically. 4-Aminopyridine enhanced the stimulation-evoked release of tritium without affecting basal release. The electrically evoked release of radioactivity was reduced by the muscarinic agonist oxotremorine and the delta selective opiate receptor agonist Metenkephalin, and was enhanced in the presence of the cholinesterase inhibitor physostigmine by the muscarinic antagonist atropine. These effects were completely abolished by 4-aminopyridine. Since 4-aminopyridine blocks potassium permeability of the neuron, it is suggested that the changes in potassium permeability and the consequent alteration of membrane polarization are involved in the presynaptic modulation of acetylcholine release.
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PMID:4-Aminopyridine interrupts the modulation of acetylcholine release mediated by muscarinic and opiate receptors. 217 82

1. The influence of castration on contraction of the guinea pig vas deferens induced by acetylcholine was investigated regarding facilitation of endogenous neurotransmitter release, changes in post-synaptic events and modification in acetylcholine metabolization. 2. Castration prolonged the duration of the isometric contraction of the vas deferens induced by acetylcholine (3 mM) but not the duration of that induced by barium chloride (10 mM). 3. Reserpinization (0.5 mg/kg) of normal and castrated guinea pigs did not change the time-course of acetylcholine-induced contraction in the vas deferens. 4. 4-Aminopyridine (0.05 mM) prolonged the contraction induced by acetylcholine and barium chloride. This effect was blocked by reserpine pretreatment, indicating that in the presence of 4-AP, both acetylcholine and barium release endogenous noradrenaline. Since there was no difference between the effects of 4-AP on organs from normal and castrated animals, prolongation of the acetylcholine-induced contraction is not related to an increase in neutransmitter release. 5. Total cholinesterase and acetylcholinesterase activities were reduced after castration and the time-course of carbachol contraction was not changed. Thus, this decrease in enzyme activity appears to play a relevant role in the prolongation of acetylcholine-induced contraction.
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PMID:The time-course of contractions induced by acetylcholine and barium in the vas deferens of normal and castrated guinea-pigs. 365 28

Cholinergic modulation of [3H]acetylcholine release evoked by electrical stimulation was studied in the rat major pelvic ganglion, which was prelabeled with [3H]choline. Acetylcholine (ACh) release was independent of the frequency of stimulation; 0.3 Hz produced the same volley output as 10 Hz. Tetrodotoxin (1 microM) or omission of Ca2+ from the medium abolished ACh release. The M1 receptor agonist (4-hydroxy-2-butynyl)-1-trimethylammonium m-chlorocarbanilate chloride (McN-A 343, 50 microM) increased release (by 136%), whereas the M2 muscarinic agonist oxotremorine (1 microM) decreased ACh release (by 22%). The muscarinic antagonists, atropine (1 microM) or pirenzepine (M1 selective, 1 microM), did not change ACh release. However, pirenzepine (1 microM) blocked the facilitatory effect of McN-A 343, and atropine (1 microM) blocked the inhibitory effect of oxotremorine. The cholinesterase inhibitor physostigmine (1-5 microM), the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP, 10 microM), and the nicotinic antagonist D-tubocurarine (50 microM) did not change ACh release. 4-Aminopyridine, a K+ channel blocker, significantly increased the release (by 146%). Seven days after decentralization of the major pelvic ganglion, the evoked release of ACh was abolished. It is concluded that release of ACh occurs from the preganglionic nerve terminals rather than from the cholinergic cell bodies and is not modulated by actions of endogenous ACh on either muscarinic or nicotinic autoreceptors. These data confirm and extend previous electrophysiological findings indicating that synapses in the major pelvic ganglion have primarily a relay function.
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PMID:Modulation of release of [3H]acetylcholine in the major pelvic ganglion of the rat. 832 60

1,2,3,4-Tetrahydro-9-aminoacridine (THA, tacrine) is a potent cholinesterase (ChE) inhibitor which is under consideration for the treatment of Alzheimer's disease. This paper examines the effect of in vivo microdialysis of THA, THB-013 (an analog of THA) and physostigmine on the extracellular concentration of acetylcholine (ACh) in the striatum of anesthetized rat, as well as their effects on in vitro striatal ChE activity. In addition, the interaction of THA and physostigmine with cholinergic receptors in rat striatum has been investigated. All three drugs inhibited ChE activity and increased the extracellular concentration of ACh in a concentration-dependent manner. In the presence of THA, atropine induced a smaller increase in extracellular ACh concentrations than it did in the presence of physostigmine, under experimental conditions in which THA (100 microM) and physostigmine (10 microM) produced an equivalent effect on ChE activity. THA bound significantly to both muscarinic and nicotinic receptors in rat striatum, whereas physostigmine did not show significant binding. THA (100 microM) and physostigmine (10 microM) produced an additive effect on the extracellular concentration of ACh, and the addition of THA (10 microM) to physostigmine (1 microM) produced further inhibition of in vitro ChE activity. 4-Aminopyridine (100 microM), a K+ channel blocker, showed no detectable effect by itself on the extracellular concentration of ACh, however, it significantly increased the extracellular concentration of ACh in the presence of physostigmine (10 microM).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of in vivo microdialysis of 1,2,3,4-tetrahydro-9-aminoacridine (THA) on the extracellular concentration of acetylcholine in the striatum of anesthetized rats. 849 22