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Dopamine D-2 Receptor Agonists Decrease the Basal Level of Inositol 1,4,5-Trisphosphate in Rat Striatal Slices

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Book cover Pharmacology and Functional Regulation of Dopaminergic Neurons

Abstract

The signal transduction mechanisms mediating the effects of dopamine are not fully elucidated. Several pieces of evidence support the concept that activation of the dopamine D-2 receptor in the neostriatum and in the anterior pituitary gland decreases adenylate cyclase (AC) activity (Enjalbert and Bockaert, 1983; Seeman and Grigoriadis, 1987; Stoof and Kebabian, 1981; Trabucchi et al., 1975). However, in more recent experiments the stimulation of the D-2 receptor was not followed by a decrease in the cyclic AMP (cAMP) level. As an example, the inhibition of the neurotensin-induced calcium influx and prolactin release in lactotrophic cells as well as the inhibition of K+-evoked dopamine release from striatal slices, both mediated by D-2 receptor stimulation, are not accompanied by changes in the cAMP levels (Memo et al., 1986a; 1986b). These findings suggest the possibility that D-2 receptors could be linked to a second messenger generating system different from the CA. For instance recent studies with striatal tissue and cells of the anterior pituitary provided evidence that dopamine, by acting at D-2 receptor sites, inhibits both AC activity (Enjalbert et al., 1986; Stoof and Kebabian, 1981) and polyphosphoinositide (PPI) breakdown. However, in a recent study with anterior pituitary cells dopaminergic stimulation did not attenuate phosphoinositide hydrolysis (Canonico et al., 1986).

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© 1988 M. Da Prada, M. Pizzi, A. Valerio, M. Memo, P.F. Spano and W.E. Haefely

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Da Prada, M., Pizzi, M., Valerio, A., Memo, M., Spano, P.F., Haefely, W.E. (1988). Dopamine D-2 Receptor Agonists Decrease the Basal Level of Inositol 1,4,5-Trisphosphate in Rat Striatal Slices. In: Beart, P.M., Woodruff, G.N., Jackson, D.M. (eds) Pharmacology and Functional Regulation of Dopaminergic Neurons. Satellite Symposia of the IUPHAR 10th International Congress of Pharmacology. Palgrave Macmillan, London. https://doi.org/10.1007/978-1-349-10047-7_11

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