The initial mode of action of copper on the cardiac physiology of the blue mussel, Mytilus edulis

• Published in: Aquatic toxicology Vol. 52; no. 1; pp. 29 - 38
• Main Authors: CURTIS, T. M, WILLIAMSON, R, DEPLEDGE, M. H
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Science 01.03.2001
• Subjects: Animal, plant and microbial ecology; Animals; Applied ecology; Biochemistry. Physiology. Immunology; Biological and medical sciences; Bivalvia - physiology; Copper - toxicity; Ecotoxicology, biological effects of pollution; Effects of pollution and side effects of pesticides on protozoa and invertebrates; Fundamental and applied biological sciences. Psychology; Heart - drug effects; Heart - physiology; Heart Rate - drug effects; Invertebrates; Mollusca; Myocardium - metabolism; Mytilus edulis; Nicotinic Antagonists - pharmacology; Physiology. Development; Reserpine - pharmacology; Heart; Cholinergic neuron; Edible mollusc; Mytilus edulis; Toxicity; Stimulation; Marine environment; Pollutant; Bivalvia; Invertebrata; Mollusca; Copper; Mechanism of action
• ISSN: 0166-445X; 1879-1514
• DOI: 10.1016/S0166-445X(00)00135-1

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. To establish if copper was directly affecting heart cell physiology, recordings of contractions from isolated ventricular strips were made using an isometric force transducer, in response to copper concentrations (as CuCl2) ranging between 1 microM and 1 mM. Inhibition of mechanical activity only occurred at 1 mM copper, suggesting that the copper-induced bradycardia observed in whole animals cannot be attributed to direct cardiotoxicity. Effects of copper on the cardiac nerves were subsequently examined. Following removal of visceral ganglia (from where the cardiac nerves originate), exposure to 12.5 microM copper had no effect on the heart rate of whole animals. The effect of copper on the heart rate of mussels could not be abolished by depletion of the monoamine content of the animal using reserpine. However, pre-treatment of the animals with alpha-bungarotoxin considerably reduced the sensitivity of the heart to copper. These results indicated that the influence of copper on the heart of M. edulis might be mediated by a change in the activity of cholinergic nerves to heart. In the final experiments, mussels were injected with either benzoquinonium or D-tubocurarine, prior to copper exposure, in an attempt to selectively block the inhibitory or excitatory cholinoreceptors of the heart. Only benzoquinonium decreased the susceptibility of the heart to copper, suggesting that copper affects the cardiac activity of blue mussels by stimulating inhibitory cholinergic nerves to the heart.