The Experts below are selected from a list of 132 Experts worldwide ranked by ideXlab platform
Susan B. Hipkens - One of the best experts on this subject based on the ideXlab platform.
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Intranigral injections of SCH 23390 inhibit SKF 82958-induced rotational behavior
Brain research, 1994Co-Authors: David M. Yurek, Susan B. HipkensAbstract:Abstract The selective D1 receptor antagonist, SCH 23390, was injected into the pars reticulata region of the lesioned substantia nigra at various concentrations (3.0, 1.5, 1.0, 0.6 or 0.3 mM) just before a s.c. injection of either the selective D1 agonist, SKF 82958; the selective D2 agonist, quinpirole; or the mixed D1–D2 receptor agonist, apomorphine. SCH 23390 pretreatment (1) had no significant effect on quinpirole rotational behavior, (2) attenuated apomorphine rotational behavior and (3) dose-dependently inhibited SKF 82958 rotational behavior with the highest SCH 23390 doses completely blocking SKF 82958 rotational behavior in some animals. These data provide further evidence that dopamine release in the midbrain may act as a neuromodulator of motor behavior, and that D1 receptors play a functional role in this process.
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Intranigral injections of SCH 23390 inhibit amphetamine-induced rotational behavior
Brain research, 1993Co-Authors: David M. Yurek, Susan B. HipkensAbstract:Rats were given unilateral 6-hydroxydopamine lesions of the nigrostriatal pathway and permanent indwelling cannula were surgically implanted into the non-lesioned side of the brain; cannula were used for direct injections of dopamine antagonists into the pars reticulata region of the non-lesioned substantia nigra. The selective D1 receptor antagonist, SCH 23390, was injected intranigrally at various concentrations (3.0, 1.5, 1.0, 0.6, or 0.3 mM) just prior to an intraperitoneal injection of amphetamine. SCH 23390 dose-dependently inhibited amphetamine-induced rotational behavior with the highest doses completely blocking rotational behavior in some animals. An intranigral injection of the selective D2 receptor antagonist, (-)-sulpiride (1.0 mM), did not produce a significant reduction in amphetamine-induced rotational behavior whereas an equivalent molar concentration of SCH 23390 (1.0 mM) produced a significant 62% reduction in amphetamine-induced rotational behavior. A concentration of SCH 23390 that produced a 50% reduction in rotational behavior when injected directly into the substantia nigra was unable to produce a significant reduction in rotational behavior when injected directly into the striatum. The effects of intranigral injections of SCH 23390 on apomorphine-induced rotational behavior were directly opposite to that observed for amphetamine-induced rotational behavior; contralateral rotational behavior increased relative to baseline measures. These data support the hypothesis that dopamine release in the midbrain may act as a neuromodulator of motor behavior, and that D1 receptors play a functional role in this process.
Hisashi Kuribara - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of methamphetamine sensitization by post-methamphetamine treatment with SCH 23390 or haloperidol
Psychopharmacology, 1995Co-Authors: Hisashi KuribaraAbstract:Methamphetamine (2 mg/kg SC) increased ambulation in mice for about 3 h, with a peak effect at around 40 min after the administration, and its repeated administration induced sensitization. Both SCH 23390 (0.03 mg/kg SC) and haloperidol (0.4 mg/kg SC), dopamine D1 and D2 receptor antagonists, respectively, completely inhibited not only the acute stimulant effect of methamphetamine but also its sensitization when repeated methamphetamine was repeatedly combined with either of these drugs. Moreover, treatment with SCH 23390 2–5 h or haloperidol 1–5 h after each methamphetamine administration significantly antagonized methamphetamine sensitization. The maximal inhibitory effect was observed in the SCHedules of 3-h post-methamphetamine treatment for both drugs. However, treatments with SCH 23390 or haloperidol at 0.5 h, 6 h and 24 h after methamphetamine had no such inhibitory effect. The mice treated with SCH 23390 or haloperidol after each saline administration (the control administration for methamphetamine) did not show significant change in the sensitivity to methamphetamine. These results suggest that methamphetamine has an effect on both dopamine D1 and D2 receptors for several hours even after cessation of its acute stimulant effect, and that such an effect is involved in the induction of sensitization to the stimulant effect of methamphetamine on ambulation in mice.
David M. Yurek - One of the best experts on this subject based on the ideXlab platform.
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Intranigral injections of SCH 23390 inhibit SKF 82958-induced rotational behavior
Brain research, 1994Co-Authors: David M. Yurek, Susan B. HipkensAbstract:Abstract The selective D1 receptor antagonist, SCH 23390, was injected into the pars reticulata region of the lesioned substantia nigra at various concentrations (3.0, 1.5, 1.0, 0.6 or 0.3 mM) just before a s.c. injection of either the selective D1 agonist, SKF 82958; the selective D2 agonist, quinpirole; or the mixed D1–D2 receptor agonist, apomorphine. SCH 23390 pretreatment (1) had no significant effect on quinpirole rotational behavior, (2) attenuated apomorphine rotational behavior and (3) dose-dependently inhibited SKF 82958 rotational behavior with the highest SCH 23390 doses completely blocking SKF 82958 rotational behavior in some animals. These data provide further evidence that dopamine release in the midbrain may act as a neuromodulator of motor behavior, and that D1 receptors play a functional role in this process.
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Intranigral injections of SCH 23390 inhibit amphetamine-induced rotational behavior
Brain research, 1993Co-Authors: David M. Yurek, Susan B. HipkensAbstract:Rats were given unilateral 6-hydroxydopamine lesions of the nigrostriatal pathway and permanent indwelling cannula were surgically implanted into the non-lesioned side of the brain; cannula were used for direct injections of dopamine antagonists into the pars reticulata region of the non-lesioned substantia nigra. The selective D1 receptor antagonist, SCH 23390, was injected intranigrally at various concentrations (3.0, 1.5, 1.0, 0.6, or 0.3 mM) just prior to an intraperitoneal injection of amphetamine. SCH 23390 dose-dependently inhibited amphetamine-induced rotational behavior with the highest doses completely blocking rotational behavior in some animals. An intranigral injection of the selective D2 receptor antagonist, (-)-sulpiride (1.0 mM), did not produce a significant reduction in amphetamine-induced rotational behavior whereas an equivalent molar concentration of SCH 23390 (1.0 mM) produced a significant 62% reduction in amphetamine-induced rotational behavior. A concentration of SCH 23390 that produced a 50% reduction in rotational behavior when injected directly into the substantia nigra was unable to produce a significant reduction in rotational behavior when injected directly into the striatum. The effects of intranigral injections of SCH 23390 on apomorphine-induced rotational behavior were directly opposite to that observed for amphetamine-induced rotational behavior; contralateral rotational behavior increased relative to baseline measures. These data support the hypothesis that dopamine release in the midbrain may act as a neuromodulator of motor behavior, and that D1 receptors play a functional role in this process.
Paul E. Mallet - One of the best experts on this subject based on the ideXlab platform.
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The dopamine receptor antagonist SCH 23390 attenuates feeding induced by Delta9-tetrahydrocannabinol.
Brain research, 2004Co-Authors: Aaron N A Verty, Iain S. Mcgregor, Paul E. MalletAbstract:A large body of evidence supports the notion that Delta9-tetrahydrocannabinol (THC) stimulates food intake by its actions on CB1 cannabinoid receptors. Indirect evidence also suggests a role for dopamine (DA) receptors in mediating THC-induced feeding. In the present study, a series of experiments involving intraperitoneal drug administration in rats were conducted to further investigate the interaction between cannabinoid and dopamine receptors in feeding behaviour. Male Wistar rats were habituated to the test environment and injection procedure, and then were injected with vehicle alone, the dopamine D1-like receptor antagonist SCH 23390 (0.005, 0.01, 0.5 or 0.1 mg/kg), THC (0.1, 0.5 or 1.0 mg/kg) or SCH 23390 and THC combined. Food intake and locomotor activity were then measured for 120 min. Results revealed that administration of SCH 23390 dose-dependently decreased food intake while THC dose-dependently increased feeding. Furthermore, SCH 23390 attenuated feeding induced by THC at a dose that did not affect feeding on its own. These findings provide direct evidence for the existence of cannabinoid-dopamine interactions in feeding behaviour and suggest that dopamine D1 signalling is necessary for cannabinoids to stimulate food intake.
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The dopamine receptor antagonist SCH 23390 attenuates feeding induced by Δ9-tetrahydrocannabinol
Brain Research, 2004Co-Authors: Aaron N A Verty, Iain S. Mcgregor, Paul E. MalletAbstract:A large body of evidence supports the notion that Δ9-tetrahydrocannabinol (THC) stimulates food intake by its actions on CB1 cannabinoid receptors. Indirect evidence also suggests a role for dopamine (DA) receptors in mediating THC-induced feeding. In the present study, a series of experiments involving intraperitoneal drug administration in rats were conducted to further investigate the interaction between cannabinoid and dopamine receptors in feeding behaviour. Male Wistar rats were habituated to the test environment and injection procedure, and then were injected with vehicle alone, the dopamine D1-like receptor antagonist SCH 23390 (0.005, 0.01, 0.5 or 0.1 mg/kg), THC (0.1, 0.5 or 1.0 mg/kg) or SCH 23390 and THC combined. Food intake and locomotor activity were then measured for 120 min. Results revealed that administration of SCH 23390 dose-dependently decreased food intake while THC dose-dependently increased feeding. Furthermore, SCH 23390 attenuated feeding induced by THC at a dose that did not affect feeding on its own. These findings provide direct evidence for the existence of cannabinoid-dopamine interactions in feeding behaviour and suggest that dopamine D1 signalling is necessary for cannabinoids to stimulate food intake.
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The dopamine receptor antagonist SCH 23390 attenuates feeding induced by Δ9-tetrahydrocannabinol
Brain Research, 2004Co-Authors: Aaron N A Verty, Iain S. Mcgregor, Paul E. MalletAbstract:A large body of evidence supports the notion that Delta9-tetrahydrocannabinol (THC) stimulates food intake by its actions on CB1 cannabinoid receptors. Indirect evidence also suggests a role for dopamine (DA) receptors in mediating THC-induced feeding. In the present study, a series of experiments involving intraperitoneal drug administration in rats were conducted to further investigate the interaction between cannabinoid and dopamine receptors in feeding behaviour. Male Wistar rats were habituated to the test environment and injection procedure, and then were injected with vehicle alone, the dopamine D1-like receptor antagonist SCH 23390 (0.005, 0.01, 0.5 or 0.1 mg/kg), THC (0.1, 0.5 or 1.0 mg/kg) or SCH 23390 and THC combined. Food intake and locomotor activity were then measured for 120 min. Results revealed that administration of SCH 23390 dose-dependently decreased food intake while THC dose-dependently increased feeding. Furthermore, SCH 23390 attenuated feeding induced by THC at a dose that did not affect feeding on its own. These findings provide direct evidence for the existence of cannabinoid-dopamine interactions in feeding behaviour and suggest that dopamine D1 signalling is necessary for cannabinoids to stimulate food intake.
William P. Smotherman - One of the best experts on this subject based on the ideXlab platform.
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Intracisternal administration of SKF-38393 and SCH-23390: behavioral effects in the rat fetus.
Pharmacology biochemistry and behavior, 1994Co-Authors: Elena I. Varlinskaya, Evgeniy S. Petrov, Scott R. Robinson, William P. SmothermanAbstract:The dopamine D1 agonist SKF-38393 and the D1 antagonist SCH-23390 were administered into the central nervous system of the E21 rat fetus via intracisternal (IC) injection. IC injection of SKF-38393 promoted a dose-dependent increase in fetal motor activity, principally including movements of the forelimbs, head, and body trunk. IC injection of SCH-23390 did not affect overall activity, but selectively suppressed forelimb, rearlimb, and head movements and promoted an increase in mouthing, licking, and facial wiping. Administration of SCH-23390 after IC injection of SKF-38393 was effective in completely reversing the behavioral effects of the D1 agonist. These findings suggest that central manipulation of dopamine D1 receptors can have direct and potent behavioral effects in the term rat fetus.
