Rapid recovery of nicotinic receptor-mediated sodium-22 influx following withdrawal from acute or chronic cholinergic stimulation
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Acetylcholine receptor-mediated uptake of22Na was studied in PC12 cells and 11-day chick muscle cells maintained in culture and exposed to carbamylcholine.
Carbamylcholine caused an initial 22-fold increase in the rate of22Na uptake but this fell to less than twice background after 4–10 min of continuous exposure. The decline reflects receptor desensitization.
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.
The lack of down-regulation in these nicotinic systems contrasts with results on muscarinic systems and may reflect different roles for these receptor types.
Key wordsnicotinic receptor carbamylcholine PC12 cells sodium influx cholinergic stimulation
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