Characterization of the binding of 3H-SCH 23390, a selective D-1 receptor antagonist ligand, in rat striatum

Billard, William; Ruperto, Vilma; Crosby, Gordon; Iorio, Louis C.; Barnett, Allen

doi:10.1016/0024-3205(84)90540-x

Cited by 562 publications

(175 citation statements)

References 8 publications

Supporting

Mentioning

152

Contrasting

Unclassified

Order By: Relevance

“…The final pellet was resuspended in 50 mM TrisHCl buffer, pH 7.4, containing 120 mM NaCl, 5 mM KCl, 2 mM CaCl 2 and 1 mM MgCl 2 . The binding assay was performed according to Billard et al (1984) with minor modifications. Briefly 400-lL aliquots of membrane preparations were incubated with different concentrations (0.03-10 nM) of [ 3 H]SCH 23390 (specific activity 80 Ci ⁄ mmol; New England Nuclear) in a final volume of 500 lL.…”

Section: Microdialysis Proceduresmentioning

confidence: 99%

Selective modifications in the nucleus accumbens of dopamine synaptic transmission in rats exposed to chronic stress

Scheggi

Leggio

Masi

et al. 2002

Journal of Neurochemistry

View full text Add to dashboard Cite

Stressful events are accompanied by modifications in dopaminergic transmission in distinct brain regions. As the activity of the neuronal dopamine (DA) transporter (DAT) is considered to be a critical mechanism for determining the extent of DA receptor activation, we investigated whether a 3-week exposure to unavoidable stress, which produces a reduction in DA output in the nucleus accumbens shell (NAcS) and medial prefrontal cortex (mPFC), would affect DAT density and DA D 1 receptor complex activity in the NAcS, mPFC and caudate-putamen (CPu). Rats exposed to unavoidable stress showed a decreased DA output in the NAcS accompanied by a decrease in the number of DAT binding sites, and an increase in the number of DA D 1 binding sites and Vmax of SKF 38393-stimulated adenylyl cyclase. In the mPFC, stress exposure produced a decrease in DA output with no modification in DAT binding or in DA D 1 receptor complex activity. Moreover, in the CPu stress exposure induced no changes in DA output or in the other neurochemical variables examined. This study shows that exposure to a chronic unavoidable stress that produces a decrease in DA output in frontomesolimbic areas induced several adaptive neurochemical modifications selectively in the nucleus accumbens.

show abstract

Section: Microdialysis Proceduresmentioning

confidence: 99%

Selective modifications in the nucleus accumbens of dopamine synaptic transmission in rats exposed to chronic stress

Scheggi

Leggio

Masi

et al. 2002

Journal of Neurochemistry

View full text Add to dashboard Cite

show abstract

“…Further, [ 3 H]SCH-23390 is not displaced from brain membranes by butyrophenones, phenothizines or other types of neuroleptics (Billard et al, 1984). Thus, this benzazepine derivative is suggested to be a specific D-1 dopamine antagonist (Hyttel, 1983).…”

Section: Introductionmentioning

confidence: 98%

“…In spite of this demonstrated specificity for the D-1 receptor (Billard et al, 1984;Molloy and Waddington, 1984;Breese et al, 1985), SCH-23390 also antagonizes the effects of directly acting dopamine agonists that are also antagonized by compounds classified as D-2 dopamine receptor antagonists (Iorio et al, 1983;Christensen et al, 1984a,b;Mailman et al, 1984;Breese et al, 1985). However, several investigators have demonstrated that the blocking action of SCH-23390 against D-2 dopamine agonists is reduced in 6-OHDAtreated rats (Christensen et al, 1984a,b;Breese et al, 1985).…”

Section: Introductionmentioning

confidence: 99%

SCH-23390 antagonism of a D-2 dopamine agonist depends upon catecholaminergic neurons

Breese

Mueller

1985

European Journal of Pharmacology

100

View full text Add to dashboard Cite

SCH-23390, a selective D-1 dopamine antagonist, was found to antagonize the locomotor stimulation induced by LY-171555, an action similar to that for haloperidol in control animals. However, this action of SCH-23390 was prevented in rats treated with 6-hydroxydopamine (6-OHDA) or with reserpine plus α-methyl-tyrosine pretreatment. These results indicate that the action of SCH-23390 to antagonize D-2 dopamine receptor actions is dependent upon functional catecholamine-containing neurons. In contrast to the lack of action of SCH-23390 to antagonize LY-171555 in 6-OHDA-treated rats, SCH-23390 blocked the locomotor stimulation induced by SKF-39393, a D-1 dopamine agonist, after this treatment. Thus, D-1 dopamine receptors are distinct from D-2 receptor sites and can exhibit a behavior similar to that observed when D-2 receptors are stimulated. These data suggest that D-1 receptor sites modulate D-2 dopamine receptor function through a mechanism dependent upon functionally intact catecholaminecontaining neurons.

show abstract

“…The supernatants were centrif uged three times at 20,000 ϫ g for 20 min (resuspending the pellet each time in 1 ml of the above buffer). The resultant pellet was resuspended, and aliquots of the suspensions were used for the determination of protein concentration according to L owry's methods (L owry et al, 1951).DA D1 receptor binding assay was performed in duplicate according to the methods of Billard et al (1984) and Bossé and Di Paolo (1996). Briefly, membrane preparations (100 g of protein in a final volume of 1 ml) were incubated with various concentrations of [ 3 H]SCH 23390 (specific activity, 83 C i /mmol; Amersham Pharmacia Biotech, Tokyo, Japan) in the above buffer at 37°C for 20 min.…”

mentioning

confidence: 99%

Chronic Stress Induces Impairment of Spatial Working Memory Because of Prefrontal Dopaminergic Dysfunction

et al. 2000

View full text Add to dashboard Cite

Although the mechanism responsible for cognitive deficits in stress-related neuropsychiatric disorders has been obscure, prefrontal cortical (PFC) dopaminergic dysfunction is thought to be involved. In animals, the mesoprefrontal dopaminergic system is particularly vulnerable to stress, and chronic stress induces working memory impairment. However, the relation between the working memory impairment and altered dopaminergic activity in chronically stressed rats is unclear. Furthermore, the change of dopaminergic activity in the PFC induced by stress is thought to express as a stress response, not as a disorder of organic function. We have previously reported that chronic stress administered by water immersion and restraint for 4 weeks induces a organic disorder such as hippocampal neuronal degeneration. We therefore examined whether chronically stressed (4 weeks) and recovered (10 d) rats show a working memory impairment caused by reduced dopamine (DA) transmission in the PFC, as suspected in the neuropsychiatric disorders. The stress impaired the spatial working memory evaluated by T-maze task and induced a marked reduction of DA transmission concomitant with an increase in DA D1 receptor density in the PFC. This memory impairment was sufficiently ameliorated by intra-PFC infusion of 10 ng SKF 81297, a D1 receptor-specific agonist. Pretreatment with intraperitoneal injection of 20 g/kg SCH 23390, a D1 receptor antagonist, reversed the SKF 81297 response. These results indicate that chronic stress induces working memory impairment through a D1 receptor-mediated hypodopaminergic mechanism in the PFC. These findings provide important information for understanding of the mechanisms underlying PFC dysfunction in stress-related neuropsychiatric disorders.Key words: chronic stress; working memory; prefrontal cortex; dopaminergic neuron; D1 receptor; cognitive deficit Exposure to stress is known to precipitate or exacerbate many neuropsychiatric disorders such as depression, Parkinson's disease, schizophrenia, and others (Schwab and Zieper, 1965;Mazure, 1995). All these disorders involve a working memory deficit caused by prefrontal cortical (PFC) dysfunction (Mattes, 1980;Weinberger et al., 1986;Deutch, 1993;Fibiger, 1995). Several antidepressants increase dopamine (DA) levels in the PFC (Tanda et al., 1994), and raising the DA level in patients with Parkinson's disease with L-3,4-dihydroxyphenylalanine improves their working memory deficit (Lange et al., 1992). These findings suggest that a reduced dopaminergic transmission in the PFC is responsible for the working memory deficits in the neuropsychiatric disorders.In animals, reduced PFC dopaminergic function or blockade of DA receptor in the PFC of monkeys and rats impairs working memory function (Brozoski et al., 1979;Simon et al., 1980;Bubser and Schmidt, 1990), which supports the observations in the neuropsychiatric disorders. In addition, an exposure to acute stress in monkeys or rats has been reported to produce working memory impairment, which can be blocked by...

show abstract

Characterization of the binding of 3H-SCH 23390, a selective D-1 receptor antagonist ligand, in rat striatum

Cited by 562 publications

References 8 publications

Selective modifications in the nucleus accumbens of dopamine synaptic transmission in rats exposed to chronic stress

Selective modifications in the nucleus accumbens of dopamine synaptic transmission in rats exposed to chronic stress

SCH-23390 antagonism of a D-2 dopamine agonist depends upon catecholaminergic neurons

Chronic Stress Induces Impairment of Spatial Working Memory Because of Prefrontal Dopaminergic Dysfunction

Contact Info

Product

Resources

About