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Aquat Toxicol
March 2001
Marine Biological Association of the UK Laboratory, Citadel Hill, PL1 2PB, Devon, Plymouth, UK.
Previous studies have shown that low levels of copper (down to 0.8 microM) induce bradycardia in the blue mussel (Mytilus edulis) and that this is not caused by prolonged valve closure. The aim of this study was to determine the precise mechanism responsible.
View Article and Find Full Text PDFParasitology
May 1995
Department of Physiology and Pharmacology, University of Southampton.
The action of two peptides isolated from the nematode Panagrellus redivivus, PF1 (SDPNFLRFamide) and PF2 (SADPNFLRFamide) have been studied on synaptic transmission in the motornervous system of the parasitic nematode Ascaris suum. Intracellular recordings were made from Ascaris somatic muscle cells and excitatory junction potentials (EJPs) elicited by stimulation of the ventral nerve cord. The EJPs were cholinergic as they were blocked by the Ascaris nicotinic receptor antagonist, benzoquinonium.
View Article and Find Full Text PDFJ Pharmacol Exp Ther
June 1993
Department of Pharmacology and Experimental Therapeutics, University of Maryland Medical School, Baltimore.
Electrophysiological and biochemical techniques were used to demonstrate that alpha-bungarotoxin-, methyllycaconitine-sensitive neuronal nicotinic acetylcholine receptors (nAChRs) can be activated via a novel agonist site(s). The residue proposed to be essential to this site is the amino acid Lys-125 of the receptor alpha subunit. In outside-out patches excised from cultured hippocampal neurons, physostigmine (PHY) and 1-methyl-PHY activated single channels whose main conductances were 46 and 23 pS.
View Article and Find Full Text PDFCell Tissue Res
August 1992
Physiological Laboratory, Faculty of Integrated Arts and Sciences, Hiroshima University, Japan.
Involvement of neuropeptides in the regulation of cardiac activity in a prosobranch mollusc, Rapana thomasiana, was studied physiologically as well as immunohistochemically. A catch-relaxing peptide (CARP) showed strong inhibitory effects on the heart with a lower threshold than acetylcholine. The action of CARP was in contrast to that of another neuropeptide, FMRFamide, which has previously been shown to enhance the heart beat.
View Article and Find Full Text PDFEur J Biochem
September 1991
Institute of Physiological Chemistry, Johannes-Gutenberg University Medical School, Mainz, Federal Republic of Germany.
We have studied the interaction of the reversible acetylcholine esterase inhibitor (-)physostigmine (D-eserine) with the nicotinic acetylcholine receptor (nAChR) from Torpedo marmorata electric tissue by means of ligand-induced ion flux into nAChR-rich membrane vesicles and of equilibrium binding. We find that (-) physostigmine induces cation flux (and also binds to the receptor) even in the presence of saturating concentrations of antagonists of acetylcholine, such as D-tubocurarine, alpha-bungarotoxin or antibody WF6. The direct action on the acetylcholine receptor is not affected by removal of the methylcarbamate function from the drug and thus is not due to carbamylation of the receptor.
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