Noradrenaline modulates oyster hemocyte phagocytosis via a beta-adrenergic receptor-cAMP signaling pathway.
Catecholamines (CA) regulate several physiological processes in molluscs. Experiments have been conducted to determine the effects of noradrenaline (NA), the principal CA circulating in bivalve hemolymph, on oyster hemocytephagocytosis. Results show that NA had a dose-dependent inhibitory effect on phagocytosis at physiological concentrations of 0.1 microM and above. The beta-adrenoceptor agonist isoproterenol mimicked the inhibitory effects of NA on phagocytosis, whereas the alpha-adrenoceptor agonist phenylephrine had no significant effect. Furthermore, the beta-adrenoceptor antagonist propanolol, but not the alpha-adrenoceptor antagonist prazosin, prevented the inhibition of phagocytosis by NA. The type IV phosphodiesterase inhibitor rolipram acted synergistically with a suboptimal concentration of isoproterenol to inhibit phagocytosis, and the protein kinase A inhibitor H-89, but not the protein kinase C inhibitor calphostin C, attenuated the effect of isoproterenol. These results show that NA can modulate oyster hemocyte phagocytosis via a beta-adrenergic receptor/cAMP/protein kinase A signaling pathway.
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Station Biologique de Roscoff, CNRS, Université Paris VI-INSU, Place Georges Teissier, Roscoff Cedex, F-29682, France.
Malham
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Cueff
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Poulet
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D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D000242:Cyclic AMP / Q000502:physiology*; D017868:Cyclic AMP-Dependent Protein Kinases / Q000037:antagonists & inhibitors / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D005434:Flow Cytometry; D006434:Hemocytes / Q000187:drug effects / Q000502:physiology*; D007545:Isoproterenol / Q000494:pharmacology; D007546:Isoquinolines / Q000494:pharmacology; D018613:Microscopy, Confocal; D009281:Naphthalenes / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology* / Q000502:physiology; D010125:Ostreidae / Q000187:drug effects / Q000502:physiology*; D010587:Phagocytosis / Q000187:drug effects*; D010656:Phenylephrine / Q000494:pharmacology; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000502:physiology; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D020889:Rolipram / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects* / Q000502:physiology; D013449:Sulfonamides
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D007546:Isoquinolines; D009281:Naphthalenes; D010726:Phosphodiesterase Inhibitors; D011943:Receptors, Adrenergic, beta; D013449:Sulfonamides; D010656:Phenylephrine; D011433:Propranolol; D000242:Cyclic AMP; D017868:Cyclic AMP-Dependent Protein Kinases; D011493:Protein Kinase C; C058819:calphostin C; D020889:Rolipram; D007545:Isoproterenol; C063509:N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; D009638:Norepinephrine; D011224:Prazosin