Abstract:
:Nicotinic agonists stimulate 22Na flux in rat pheochromocytoma PC12 cells. The stimulatory effect of carbamylcholine is maximal at 1 mM, while the stimulatory effect of nicotine and anatoxin maximize at the same level at 100 microM and 10 microM, respectively. The tertiary amines arecolone and isoarecolone have no effect on flux at 100 microM, while the methiodides at 100 microM stimulate flux to an extent similar to 1 mM carbamylcholine. Dihydro and alcohol analogues of isoarecolone methiodide have markedly smaller effects on flux. A preincubation for 2 to 20 min with carbamylcholine (2 mM), nicotine (300 microM), anatoxin (30 microM) or isoarecolone methiodide (100 microM) causes marked desensitization to a subsequent carbamylcholine-elicited stimulation of flux. d-Tubocurarine, mecamylamine, hexamethonium, and chlorisondamine inhibit carbamylcholine-elicited flux with IC50 values of 1.0, 0.8, 43, and 0.020 microM, respectively. Atropine has no effect at 1 microM, but reduces the response to carbamylcholine by 50% at 8.6 microM, presumably as a noncompetitive blocker. Other noncompetitive blockers of nicotinic acetylcholine-receptors, such as histrionicotoxins, gephyrotoxin, pumiliotoxin C, phencyclidine, bupivacaine and piperocaine, inhibit carbamylcholine-elicited stimulation of 22Na flux with IC50 values from 0.3 to 1.8 microM. In contrast to d-tubocurarine, which inhibits carbamylcholine-elicited desensitization, and mecamylamine, which has no apparent effect on desensitization, chlorisondamine and certain noncompetitive blockers appear to enhance desensitization. The effects of agonists, antagonists and noncompetitive blockers at the neuronal nicotinic acetylcholine receptor-channel of PC12 cells are compared to their effects on binding of [125I]alpha-bungarotoxin to agonist-recognition sites and of [3H]perhydrohistrionicotoxin to noncompetitive blocker sites of the nicotinic acetylcholine receptor-channel of electric ray (Torpedo) electroplax membranes. There are marked differences in relative potencies for the two types of nicotinic acetylcholine receptor-channel.
journal_name
Neurochem Resjournal_title
Neurochemical researchauthors
Daly JW,Nishizawa Y,Edwards MW,Waters JA,Aronstam RSdoi
10.1007/BF00965571subject
Has Abstractpub_date
1991-04-01 00:00:00pages
489-500issue
4eissn
0364-3190issn
1573-6903journal_volume
16pub_type
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