Pharmacological and Immunofluorescence Identification of Dopamine D2 Receptors in the Lateral Ciliated Cells of the Gill of the Bivalve Mollusc Crassostra virginica


Meeting Abstract

P2.95  Tuesday, Jan. 5  Pharmacological and Immunofluorescence Identification of Dopamine D2 Receptors in the Lateral Ciliated Cells of the Gill of the Bivalve Mollusc Crassostra virginica ANADOR, S.*; BROWN, C.; LICORISH, R.; CILLI, N.; FLEMING, R.; CARROLL, M.A.; CATAPANE, E.J.; Medgar Evers College, Brooklyn catapane@mec.cuny.edu

Lateral cell cilia of gill of Crassostra virginicaare controlled dopamine (DA) and serotonin (HT) nerves originating from the cerebral and visceral ganglia. DA slows down beating of lateral cilia and serotonin accelerates them. We undertook a pharmacological and immunofluorescence study of DA receptors. DA receptors are classified as D1-like and D2-like, each with subtypes. D1-like are coupled to G protein Gαs and activates adenylate cyclase. D2-like are coupled to the G protein Gαi, and inhibits formation of cAMP by inhibiting adenylate cyclase. Beating of cilia were measured by stroboscopic microscopy. D1 and D2 agonists and antagonists were applied to gill to determine their efficacy in altering beating. D2 agonist were effective in mimicking DA, and D2 antagonists were effective in blocking the actions of DA. D1 agonist and antagonist did not alter the beating of the cilia nor block the effects of DA. We further examined the receptor by using a primary antibody against D2 receptors followed by an FITC linked secondary antibody to visualize them. Gill was exposed to antibodies and prepared for light microscope. Control sections without primary antibody exposure were similarly treated and viewed. Antibody treated sections showed bright FITC fluorescence in the lateral ciliated cells and other areas of gill. Control sections did not. The study shows postsynaptic DA receptors involved in the cilio-inhibitory response of the lateral cells of gill are D2 type. The study also shows this preparation is a good model for pharmacological studies of DA function as well as the pharmacology of drugs affecting biogenic amines. This work was supported by grants 2R25GM0600305 of NIGMS, 0516041071 of NYSDOE, 0622197 of NSF and P382A080040 of the USDE.

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