Rapid recovery of nicotinic receptor-mediated sodium-22 influx following withdrawal from acute or chronic cholinergic stimulation.
1. Acetylcholine receptor-mediated uptake of 22Na was studied in PC12 cells and 11-day chick muscle cells maintained in culture and exposed to carbamylcholine. 2. Carbamylcholine caused an initial 22-fold increase in the rate of 22Na uptake but this fell to less than twice background after 4-10 min of continuous exposure. The decline reflects receptor desensitization. 3. The effects of acute (10-min) and chronic (10-day) exposure were compared in order to determine whether there was a down-regulation of acetylcholine receptors on chronic exposure to carbamylcholine. No down-regulation was observed on either PC12 or muscle cells. 4. The lack of down-regulation in these nicotinic systems contrasts with results on muscarinic systems and may reflect different roles for these receptor types.
D000310:Adrenal Gland Neoplasms / Q000378:metabolism; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002217:Carbachol / Q000494:pharmacology*; D002460:Cell Line; D002642:Chick Embryo; D009132:Muscles / Q000378:metabolism*; D010673:Pheochromocytoma / Q000378:metabolism; D011950:Receptors, Cholinergic / Q000378:metabolism*; D011978:Receptors, Nicotinic / Q000187:drug effects / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*
D011950:Receptors, Cholinergic; D011978:Receptors, Nicotinic; D002217:Carbachol; D012964:Sodium