These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Receptor protection studies to characterize neuronal nicotinic receptors: tubocurarine prevents alkylation of adrenal nicotinic receptors.
    Author: Free RB, McKay DB.
    Journal: Brain Res; 2001 Feb 09; 891(1-2):176-84. PubMed ID: 11164821.
    Abstract:
    Our laboratory has evidence that multiple nicotinic acetylcholine receptor subtypes regulate bovine adrenal catecholamine release. In the following studies, receptor protection assays were used to differentiate adrenal nicotinic receptor subpopulations. Under alkylating conditions, bromoacetylcholine (30 microM) reduced nicotinic receptor-stimulated adrenal catecholamine secretion by approximately 80%. When 100 microM tubocurarine was present during alkylation, nicotine-stimulated secretion was reduced by less than 30%. Hexamethonium (500 microM), decamethonium (500 microM), mecamylamine (50 microM), pentolinium (50 microM), adiphenine (50 microM), methyllycaconitine (1 microM) and alpha-bungarotoxin (1 microM) afforded no protection when present during alkylation. When the pharmacology of residual, tubocurarine-protected receptors was investigated, the EC50 value for nicotine's stimulatory effects on secretion significantly increased from 4.0 (2.5-6.5) microM in control cells to 9.1 (7.2-11.4) microM in tubocurarine-protected cells. In addition, the IC50 value for tubocurarine's inhibitory effects on release significantly decreased from 0.7 (0.5-0.9) microM in control cells to 0.3 (0.2-0.4) microM in tubocurarine-protected cells. These studies support the use of protection assays to characterize nicotinic receptor subpopulations.
    [Abstract] [Full Text] [Related] [New Search]