Rapid recovery of nicotinic receptor-mediated sodium-22 influx following withdrawal from acute or chronic cholinergic stimulation
- PMID: 7159905
- PMCID: PMC11572808
- DOI: 10.1007/BF00711153
Rapid recovery of nicotinic receptor-mediated sodium-22 influx following withdrawal from acute or chronic cholinergic stimulation
Abstract
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.
References
-
- Brown, D. A., and Fumigalli, L. (1977). Alpha-bungarotoxin binding and receptor block in rat superior cervical ganglion.Brain Res.129165–168.
-
- Burt, D. R., Creese, I., and Snyder, S. H. (1977). Antischizophrenic drugs. Chronic treatment elevates dopamine receptors binding in brain.Science196624–625. - PubMed
-
- Catterall, W. A. (1975). Sodium transport by the acetylcholine receptor of cultured muscle cells.J. Biol. Chem.2501776–1781. - PubMed
-
- Fischbach, G. D. (1972). Synapse formation between dissociated nerve and muscle cells in low density cultures.Dev. Biol.28407–429. - PubMed
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources