SCH 23390 may alter dopamine-mediated motor behaviour via striatal D-1 receptors

Boyce, Susan; Kelly, Eamonn; Davis, Alan; Fleminger, Simon; Jenner, Peter; Marsden, C. D.

doi:10.1016/0006-2952(85)90632-x

Cited by 36 publications

(10 citation statements)

References 12 publications

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“…Furthermore, SCH-23390 was ineffective in further decreasing dopamine agonist-induced yawning in reserpinized animals, and yet attenuated the yawning induced by B-HT 920 (a selective dopamine autoreceptor agonist in non-denervated animals; Anden et al 1982), even in animals with kainate lesions of the striatum (Longoni et al 1987). These findings suggest to us that DI and D2 receptors may be coupled presynaptically as well as postsynaptically, as has been previously suggested by others (Boyce et al 1985;Pugh et al 1985;Carlson et al 1987).…”

Section: Discussionsupporting

confidence: 57%

Apomorphine-induced yawning in rats is abolished by bilateral 6-hydroxydopamine lesions of the substantia nigra

1987

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Apomorphine-induced yawning was studied in male rats with bilateral 6-hydroxydopamine lesions of the substantia nigra. Apomorphine 10, 20 and 50 micrograms/kg SC induced dose-dependent yawning in unoperated controls and animals with sham lesions. In the lesioned animals (in which the mean striatal dopamine depletion was 67%), the maximum yawning response rate was greatly attenuated with no evidence that the dose response curve was shifted in either direction. Furthermore, blockade of yawning in the lesioned animals was not simply due to suppression by other stereotyped behaviours, since there was no evidence of increased sniffing or chewing in these animals. These data provide further support for the hypothesis that apomorphine-induced yawning is mediated by dopamine autoreceptors and requires intact nigrostriatal projections.

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Section: Discussionsupporting

confidence: 57%

Apomorphine-induced yawning in rats is abolished by bilateral 6-hydroxydopamine lesions of the substantia nigra

1987

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“…SCH 23390 fails to increase prolactin levels in rats (Iorio et al, 1983;Saller and Salama, 1986b), suggesting that it does not possess significant affinity for the prototype D2 receptor. Consistent with this proposal is the report of Hyttel (1983) showing that SCH 23390 is considerably more potent as a displacer of specific binding of 3H-cis(Z)-pitflutixol to D1 rece tors (Ki=1.3 nM) than 3H-spiperone (Ki=880 receptors in striatal membranes (see also Boyce et al, 1985;Cross et al, 1983;Saller and Salama, 1986a). However, a lower selectivity ratio (approximately 10) has been suggested when the DA receptor-regulated control of ACh release in striatal slices is used as a measure of D2 receptor activity (Plantj6 et al, 1984b; see also Hyttel, 1984).…”

Section: Bsupporting

confidence: 56%

“…Unlike D2 receptor antagonists (Carlsson, 1978;Magnusson et al, 1986), SCH 23390 does not increase the affinity of tyrosine hydroxylase for the pterin cofactor (Onali et al, 1985a) and, in addition, produces only a small increase (30-50%) in striatal DA synthesis, and metabolite (DOPAC and HVA) levels (Boyce et al, 1985;Hjorth and Carlsson, 1987a;Iorio et al, 1983;Onali et al, 1985a;Saller and Salama, 1986a). The latter small effect may reflect an affinity of SCH 23390 for postsynaptic DA receptors without a corresponding effect at DA autoreceptors (cf.…”

Section: Dopamine Autoreceptorsmentioning

confidence: 99%

Review: D1 dopamine receptor—the search for a function: A critical evaluation of the D1/D2 dopamine receptor classification and its functional implications

Clark

White

1987

Synapse

652

226

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The present review focuses on the hypothesized D1/D2 dopamine (DA) receptor classification, originally based on the form of receptor coupling to adenylate cyclase activity. The pharmacological effects of compounds exhibiting putative selective agonist or antagonist profiles at those DA receptors positively coupled to adenylate cyclase activity (D1 DA receptors) are extensively reviewed. Comparisons are made with the effects of putative selective D2 DA receptor agonists and antagonists, and on the basis of this work, the DA receptor classification is critically evaluated. A variety of biochemical, behavioral, and electrophysiological evidence is presented which supports the view that D1 and D2 DA receptors can interact in both an opposing and synergistic fashion. Particular attention is focused on the possibility that D1 receptor stimulation is required to enable the expression of certain D2 receptor-mediated effects, and the functional consequences of this form of interaction are considered. A hypothetical model is presented which considers how both the opposing and enabling forms of interaction between D1 and D2 DA receptors can control behavioral expression. Finally, the clinical relevance of this work is discussed and the potential use of selective D1 receptor agonists and antagonists in the treatment of psychotic states and Parkinson's disease is considered.

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“…Reduction of D, receptor activation produced by acute DA depletion abolishes the characteristic behavioral effects (enhanced locomotor activity and stereotyped sniffing) of selective D, agonists; coadministration of a D, agonist reinstates these behaviors (Gershanik et al, 1983;Braun and Chase, 1986;Jackson and Hashizume, 1986;Longoni et al, 1987;Walters et al, 1987;Meller et al, 1988;White et al, 1988). In addition, D, receptor blockade abolishes these behavioral effects of both mixed D,/D, agonists (Christensen et al, 1984;Mailman et al, 1984;Arm, 1985a;Boyce et al, 1985;Schulz et al, 1985) and selective D, agonists in the presence of normal DA tone (Amt, 1985a;Breese and Meuller, 1985;Molloy and Waddington, 1985;Pugh et al, 1985;Longoni et al, 1987;Walters et al, 1987). In contrast, D, receptor antagonists fail to block the effects of both mixed D,/D, agonists and selective D, agonists in behavioral models utilizing rats with supersensitive DA receptors (Amt, 1985b, Amt andHyttel, 1985;Breese and Meuller, 1985).…”

mentioning

confidence: 99%

Lesions of the nigrostriatal dopamine projection increase the inhibitory effects of D1 and D2 dopamine agonists on caudate-putamen neurons and relieve D2 receptors from the necessity of D1 receptor stimulation

et al. 1990

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Extracellular single unit recording and microiontophoretic techniques were used to determine the sensitivities and interactions of D1 and D2 dopamine (DA) receptors in the caudate putamen (CPu) of rats that were denervated of DA by intraventricular injections of the catecholamine neurotoxin 6-hydroxydopamine (6-OHDA). Seven to 10 d after the 6-OHDA injection, DA levels in the ipsilateral CPu were reduced to 11.8% of control. Current-response curves revealed that the inhibitory responses of CPu neurons to microiontophoretic administration of both the selective D1 receptor agonist SKF-38393 and the selective D2 receptor agonist quinpirole were significantly increased in 6-OHDA-pretreated rats, suggesting up-regulation of both receptor subtypes. Although our previous studies have established that D1 receptor activation is normally required for (enables) the inhibitory effects of selective D2 agonists in the CPu, this requirement was no longer evident in 6-OHDA- denervated rats. Whereas acute DA depletion [produced by the tyrosine hydroxylase inhibitor alpha-methyl-p-tyrosine (AMPT)] attenuated the inhibitory effects of quinpirole on CPu neurons, long-term DA denervation (produced by 6-OHDA) enhanced the inhibitory effects of the D2 agonist. The enhanced effects of quinpirole in 6-OHDA-lesioned rats were not due to residual DA stimulating supersensitive D1 receptors (i.e., enabling) since further DA depletion (99.7%), produced by acute administration of AMPT in 6-OHDA-lesioned rats, failed to diminish the inhibitory efficacy of quinpirole. In addition to relieving D2 receptors from the need for D1 receptor-mediated enabling, 6-OHDA lesions also abolished the normal synergistic relationship between the receptor subtypes since low (subinhibitory) currents of SKF-38393 (4 nA) failed to potentiate the inhibitory effects of quinpirole on CPu neurons in lesioned rats. Similar findings (i.e., supersensitivity and loss of synergistic effects) were obtained from rats that had received repeated pretreatment with reserpine (2.5 mg/kg) for 4 d, indicating that these effects of 6-OHDA lesions were due to the depletion of synaptic DA rather than to the structural loss of DA terminals. Therefore, both the quantitative (potentiation) and the qualitative (enabling) synergistic effects between D1 and D2 receptors in the rat CPu were abolished when these receptors were functionally supersensitive. The present study provides electrophysiological support for previous behavioral studies indicating that the requirement of D1 receptor stimulation for D2 receptor-mediated functional effects (enabling) is not maintained in rats chronically depleted of DA by either 6-OHDA lesions or repeated reserpine.

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SCH 23390 may alter dopamine-mediated motor behaviour via striatal D-1 receptors

Cited by 36 publications

References 12 publications

Apomorphine-induced yawning in rats is abolished by bilateral 6-hydroxydopamine lesions of the substantia nigra

Apomorphine-induced yawning in rats is abolished by bilateral 6-hydroxydopamine lesions of the substantia nigra

Review: D1 dopamine receptor—the search for a function: A critical evaluation of the D1/D2 dopamine receptor classification and its functional implications

Lesions of the nigrostriatal dopamine projection increase the inhibitory effects of D1 and D2 dopamine agonists on caudate-putamen neurons and relieve D2 receptors from the necessity of D1 receptor stimulation

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