Rapid recovery of nicotinic receptor-mediated sodium-22 influx following withdrawal from acute or chronic cholinergic stimulation

Robert G. Siman*, William L. Klein

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

1. Acetylcholine receptor-mediated uptake of22Na 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 of22Na 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.

Original languageEnglish (US)
Pages (from-to)255-261
Number of pages7
JournalCellular and molecular neurobiology
Volume2
Issue number3
DOIs
StatePublished - Sep 1 1982

Keywords

  • PC12 cells
  • carbamylcholine
  • cholinergic stimulation
  • nicotinic receptor
  • sodium influx

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Cell Biology

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