Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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