Differential regulation of muscarinic and nicotinic receptors by cholinergic stimulation in cultured avian retina cells

Robert G. Siman, William L. Klein*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

13 Scopus citations


Sustained cholinergic stimulation of retina cells grown in primary aggregate and monolayer cultures regulated the concentration of muscarinic but not nicotinic receptors. Muscarinic receptor sites, quantified by the binding of [3H]quinuclidinyl benzilate to membranes and the binding of [3H]N-methyl-scopolamine to intact cells, decreased up to 84% following long-term incubation of cultures in muscarinic agonists. This decrease was blocked by atropine and was not induced by chronic nicotine treatment. The rate of the muscarinic response was biphasic. A rapid binding decrease of 30% occurred within 15 min. The slower phase was half-maximal by 6 h and was complete by 24 h. Neither the fast nor the slow receptor loss was reversed by the guanine nucleotide GppNp. Three different depolarizing agents (gramicidin D, protoveratrine, and ouabain) blocked the cholinergic-induced receptor loss, but the hyperpolarizing ionophore valinomycin had no effect. In contrast to the muscarinic response, nicotinic receptor binding was not altered by chronic receptor stimulation. Exposure to receptor-saturating doses of carbamylcholine or nicotine for 48 h did not change [125I]α-bungarotoxin or [3H]bromoacetylcholine binding. Differential regulation of acetylcholine receptors is discussed in relation to the possible physiological role of receptor regulation by receptor activity.

Original languageEnglish (US)
Pages (from-to)99-108
Number of pages10
JournalBrain research
Issue number1
StatePublished - Feb 28 1983


  • cholinergic receptor
  • modulation
  • muscarinic receptor
  • nicotinic receptor
  • retina
  • synapse

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology


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