Serotonin-Stimulated Adenylate Cyclase in the Gill of a Freshwater Mussel and Its Relationship to Sodium Transport

Abstract

The freshwater bivalve Ligumia subrostrata exhibited a two- to threefold increase in the unidirectional influx of sodium when injected with serotonin (5-HT) or dibutyryl cAMP, a response similar to that of an animal depleted of sodium. The serotonin-dependent stimulation of the sodium influx was dose dependent. The Na net flux was directly related to the endogenous cAMP concentration observed in the gill tissue, the principal site of sodium transport in freshwater mussels. The majority of gill adenylate cyclase (AC) activity was located in the pellet of crude gill homogenate (basal activity 21.81 pmol [mg protein · 5 min]-1), exhibited halide stimulation (up to tenfold basal activity), and required 0.1 mM GTP. Gill pellet adenylate cyclase was stimulated by serotonin and dopamine but not L-dopa, octopamine, norepinephrine, and epinephrine. The gill AC exhibited maximally stimulated activity (2–3 × basal) in the presence of serotonin and dopamine, with half-maximal stimulation occurring at 3.0 μM/liter for 5-HT and 1.0 μM/liter for dopamine. Cyproheptadine, a serotonin antagonist, inhibited the 5-HT-dependent increase in adenylate cyclase activity. The dopamine antagonist, chlorpromazine, inhibited dopamine-stimulated gill AC activity. Prostaglandin E2 (0.2 μg/ml) did not modify either basal or 5-HT-stimulated adenylate cyclase activity. Gill pellet adenylate cyclase activity from mussels maintained for over 4 wk in deionized water was not different from pond water-acclimated mussels.