Noradrenaline modulates oyster hemocyte phagocytosis via a beta-adrenergicreceptor-cAMP signaling pathway

Citation
A. Lacoste et al., Noradrenaline modulates oyster hemocyte phagocytosis via a beta-adrenergicreceptor-cAMP signaling pathway, GEN C ENDOC, 122(3), 2001, pp. 252-259
Citations number
42
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
GENERAL AND COMPARATIVE ENDOCRINOLOGY
ISSN journal
00166480 → ACNP
Volume
122
Issue
3
Year of publication
2001
Pages
252 - 259
Database
ISI
SICI code
0016-6480(200106)122:3<252:NMOHPV>2.0.ZU;2-2
Abstract
Catecholamines (CA) regulate several physiological processes in molluscs. E xperiments have been conducted to determine the effects of noradrenaline (N A), the principal CA circulating in bivalve hemolymph, on oyster hemocyte p hagocytosis. Results show that NA had a dose-dependent inhibitory effect on phagocytosis at physiological concentrations of 0.1 muM and above. The bet a -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 prop anolol, but not the alpha -adrenoceptor antagonist prazosin, prevented the inhibition of phagocytosis by NA. The type IV phosphodiesterase inhibitor r olipram acted synergistically with a suboptimal concentration of isoprotere nol to inhibit phagocytosis, and the protein kinase A inhibitor H-89, but n ot the protein kinase C inhibitor calphostin C, attenuated the effect of is oproterenol. These results show that NA can modulate oyster hemocyte phagoc ytosis via a beta -adrenergic receptor/cAMP/protein kinase A signaling path way. (C) 2001 Academic Press.