Tuning Wasp Toxin Structure for Nicotinic Receptor Antagonism: Cyclohexylalanine-Containing Analogues as Potent and Voltage-Dependent Blockers

ChemMedChem ◽  
2006 ◽  
Vol 1 (3) ◽  
pp. 303-305 ◽  
Author(s):  
Christian A. Olsen ◽  
Ian R. Mellor ◽  
Petrine Wellendorph ◽  
Peter N. R. Usherwood ◽  
Matthias Witt ◽  
...  
Keyword(s):  
Nicotinic Receptor ◽  
Receptor Antagonism ◽  
Voltage Dependent

scholarly journals Cover Picture: Tuning Wasp Toxin Structure for Nicotinic Receptor Antagonism: Cyclohexylalanine-Containing Analogues as Potent and Voltage-Dependent Blockers (ChemMedChem 3/2006)

ChemMedChem ◽  
2006 ◽  
Vol 1 (3) ◽  
pp. 281-281
Author(s):  
Christian A. Olsen ◽  
Ian R. Mellor ◽  
Petrine Wellendorph ◽  
Peter N. R. Usherwood ◽  
Matthias Witt ◽  
...  
Keyword(s):  
Nicotinic Receptor ◽  
Receptor Antagonism ◽  
Voltage Dependent

Effect of Muscarinic and Nicotinic Receptor Antagonism on Rat Gastric Motor Activity

Pharmacology ◽  
2010 ◽  
Vol 85 (5) ◽  
pp. 272-279 ◽  
Author(s):  
Pieter Janssen ◽  
Lisa K.C. Karlsson ◽  
Maria Astin Nielsen ◽  
Per-Göran Gillberg ◽  
Leif Hultin
Keyword(s):  
Motor Activity ◽  
Nicotinic Receptor ◽  
Receptor Antagonism ◽  
Gastric Motor Activity

scholarly journals Patterns of nicotinic receptor antagonism II: Cardiovascular effects in rats

2013 ◽  
Vol 131 (3) ◽  
pp. 284-297 ◽  
Author(s):  
Emily M. Jutkiewicz ◽  
Kenner C. Rice ◽  
F. Ivy Carroll ◽  
James H. Woods
Keyword(s):  
Nicotinic Receptor ◽  
Cardiovascular Effects ◽  
Receptor Antagonism

Ion channels and membrane potential in stimulus–secretion coupling in adrenal paraneurons

1984 ◽  
Vol 62 (5) ◽  
pp. 477-483 ◽  
Author(s):  
Daniel L. Kilpatrick
Keyword(s):  
Membrane Potential ◽  
Ion Channels ◽  
Adrenal Medulla ◽  
Nicotinic Receptor ◽  
Calcium Influx ◽  
Inhibitory Effect ◽  
Muscle Membrane ◽  
Bovine Adrenal Medulla ◽  
Voltage Dependent ◽  
Stimulus Secretion Coupling

Cultured bovine adrenal medulla cells have been shown to contain several different ion channels (Na+, Ca2+ acetylcholine receptor regulated) whose activation leads to the secretion of catecholamines. The pharmacology of these ion channels and their interactions during secretion have been examined. The mechanisms of agonist-induced calcium influx are of particular interest since this is an early obligatory event during secretion from the adrenal medulla. Data obtained on catecholamine release and 45Ca2+ uptake indicate that both voltage-dependent and voltage-independent calcium influx mechanisms operate in cultured bovine adrenal medulla cells. The significance of these results in understanding the mechanism of action of the physiological stimulus acetylcholine (Ach) will be discussed. The alkaloid channel neurotoxins D-600, batrachotoxin, veratridine, and aconitine were shown to exert a noncompetitive inhibitory effect on Ach-induced ion flux in adrenal medulla cells, presumably through an interaction with the nicotinic receptor regulated channel. Lipid-soluble neurotoxins may interact with multiple ion channels in nerve and muscle membrane.

scholarly journals Noncompetitive, Voltage-Dependent NMDA Receptor Antagonism by Hydrophobic Anions

2012 ◽  
Vol 83 (2) ◽  
pp. 354-366 ◽  
Author(s):  
Andrew J. Linsenbardt ◽  
Mariangela Chisari ◽  
Andrew Yu ◽  
Hong-Jin Shu ◽  
Charles F. Zorumski ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonism ◽  
Voltage Dependent

Role of [Na+]i and [Ca2+]i in nicotine-induced norepinephrine release from bovine adrenal chromaffin cells

1995 ◽  
Vol 269 (3) ◽  
pp. C572-C581 ◽  
Author(s):  
S. H. Gerber ◽  
A. Haunstetter ◽  
C. Kruger ◽  
A. Kaufmann ◽  
R. Nobiling ◽  
...  
Keyword(s):  
Nicotinic Receptor ◽  
Chromaffin Cells ◽  
Sodium Concentration ◽  
Release Mechanism ◽  
Adrenal Chromaffin Cells ◽  
Sodium Influx ◽  
Voltage Dependent ◽  
Adrenal Chromaffin

Intracellular free sodium ([Na+]i) and calcium ([Ca2+]i) concentrations were determined by sodium-binding benzofuran isophthalate (SBFI) and fura 2 microfluorimetry, respectively, in bovine adrenal chromaffin cells (BCC). Validation of SBFI microfluorimetry by in vitro and in vivo calibration revealed a reliable assessment of [Na+]i within a range of 1-30 mM in single BCC. Nicotine (0.1-10 microM) induced concentration-dependent increases of both [Na+]i (from 3.3 +/- 0.1 to 25.6 +/- 0.4 mM, n = 76, P < 0.001) and [Ca2+]i (from 64 +/- 1 to 467 +/- 16 nM, n = 87, P < 0.001), which were accompanied by an increase in [3H]norepinephrine (NE) release. Consistent with an exocytotic release mechanism, nicotine-induced increments of [Ca2+]i and [3H]NE release were reduced under calcium-free conditions and by gadolinium chloride (40 microM), whereas [Na+]i was not affected. In contrast, a parallel attenuation of nicotine-evoked changes in [Na+]i, [Ca2+]i, and [3H]NE release was observed during reduction of the extracellular sodium concentration. The nicotine-evoked responses were neutralized by the nicotinic receptor antagonist hexamethonium (100 microM) but not by blockade of voltage-dependent sodium channels (1 microM tetrodotoxin). In conclusion, the nicotine-induced exocytotic release of [3H]NE is triggered by an increase in [Ca2+]i, which is facilitated by sodium influx through the nicotinic receptor ionophore.

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