Expression of striatal D1 dopamine receptors coupled to inositol phosphate production and Ca2+ mobilization in Xenopus oocytes.

Abstract

Expression of central nervous system receptors for dopamine was examined by i jection of poly(A)+ RNA (mRNA) from rat striatum into oocytes from Xenopus laevis. Electrophysiological measurements in mRNA-injected oocytes indicated that addition of 100 ,IM dopamine induced an inward current (40-100 nA) that was consistent with the activation of endogenous Ca2+-dependent Cl-channels. This current was also elicited by addition of the selective DI agonist SKF 38393 but not by the selective D2 agonist quinpirole. Prior addition of the dopaminergic antagonist cis-piflutixol completely abolished dopamine-induced currents but had no effect on currents produced by serotonin. Using 4Ca2' efflux assays, addition of 100 FLM dopamine to injected oocytes stimulated efflux 2-to tTo whom reprint requests should be addressed. 2196The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" ein accordance with 18 U.S.C. §1734 solely to indicate this fact.

Agonist-Specific Coupling of a ClonedDrosophila melanogasterD1-Like Dopamine Receptor to Multiple Second Messenger Pathways by Synthetic Agonists

“…Thus, a range of cloned D1-like receptor subtypes did not couple to inositol phosphate effects when expressed in C OS-7 , baby hamster kidney cells, or Chinese hamster ovary (CHO) (Pedersen et al, 1994) cells, but they did affect calcium metabolism when expressed in L tk cells (Bouvier et al, 1993). In addition, D1-dopamine receptors coupled to both inositol phosphate production and C a 2ϩ mobilization when rat striatal mRNA was injected into Xenopus oocytes, giving inward currents caused by the activation of the endogenous calcium-dependent chloride current, similar to those observed in the present study (Mahan et al, 1990). Further, a cloned, truncated D1-like dopamine receptor from goldfish retina both stimulated cAM P production and increased intracellular calcium mobilization when expressed in HEK 293 cells (Frail et al, 1993).…”

A primordial dopamine D1‐like adenylyl cyclase‐linked receptor from Drosophila melanogaster displaying poor affinity for benzazepines

“…These receptors have typically been classified as Dl-like (D1, D1B/D5) or D2-1ike (D2, D3, D4) based on pharmacological, biochemical and structural criteria (for reviews see [3][4][5]). The recent cloning of the D1C receptor from Xenopus laevis [6] and D 1D receptor from Gallus domesticus [7] confirm that the the Dl-like receptor family is as heterogeneous and complex as pharmacological, behavioural and/or biochemical data suggest [8][9][10][11][12][13][14].…”

Activation of the 5‐HT1c receptor expressed in Xenopus oocytes by the benzazepines SCH 23390 and SKF 38393

“…Others, however, reported that neither mianserin nor ketanserin inhibited the response to dopamine or SKF 38393 (Mahan et al, 1990;Sakai et al, 1990), and it was suggested (Mahan et al, 1990) that the responses may be due to activation of Dl-receptors thought to be coupled to phosphatidylinositol hydrolysis in mammalian cells (Undie & Friedman, 1990;Felder et al, 1989a,b; but see Dyck, 1990;Rubinstein & Hitzemann, 1990 (Molloy & Waddington, 1987;LaHoste & Marshall, 1990). It may be of interest to determine if such responses were due to the activation of 5-HT1c or receptors, particularly since the 5-HT1c receptor recently has been found to occur in many regions of the brain outside of the choroid plexus (Hoyer et al, 1986a-;Hoffman & Mezey, 1989;Molineaux et al, 1989;Mengod et al, 1990).…”

“…The response to SCH 23390 in 5-HT1c oocytes, unlike the responses to the other benzazepines and 5-HT, activated slowly and often required several minutes of exposure to the compound. The rate of association of SCH 23390 with the dopamine D1-receptor is relatively slow (Billard et al, 1984;Andersen et al, 1985;Niznik et al, 1986 However, SKF 77434 (100gM) and SKF 82958 (100pM) (Hyttel, 1983;Hicks et al, 1984;Ohlstein & Berkowitz, 1985;Hess et al, 1986;Bischoff et al, 1986;McQuade et al, 1988;De Keyser et al, 1989 (Sumikawa et al, 1984;Mahan et al, 1990;Sakai et al, 1990). …”