Short communication5HT-receptor antagonist properties of SCH 23390 in vascular smooth muscle and brain
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Cited by (94)
Microinjections of a dopamine D1 receptor antagonist into the ventral tegmental area block the expression of cocaine conditioned place preference in rats
2014, Behavioural Brain ResearchCitation Excerpt :Therefore, it is possible that intra-VTA microinjections of SCH 23390 reduced the expression of cocaine CPP by reducing DA cell activity and release through blockade of DA somatic D5 receptors. SCH 23390 also can act as an agonist at 5-HT2c receptors [93–97]. Thus, the observed results of intra-VTA injections of SCH 23390 on cocaine CPP might be due to 5-HT2c receptor agonist action.
Involvement of adenosine A<inf>2A</inf> and dopamine receptors in the locomotor and sensitizing effects of cocaine
2006, Brain ResearchCitation Excerpt :This result differs from the previous finding of White et al. (1998) who have shown that SCH 23390 reduced the expression of cocaine sensitization, but a higher dose of SCH 23390 (0.5 mg/kg) was used in that experiment. It should be added that SCH 23390, apart from its affinity for DA D1R resulting in D1 antagonistic activity (Borsini et al., 1995; Hall et al., 1986), displays in in vitro functional assays either agonistic (Briggs et al., 1991) or antagonistic (Hicks et al., 1984; Hoyer et al., 1989) activity at 5-HT2 receptors which suggests also the contribution of these receptors in the action of SCH 23390. Since 5-HT2 receptors have a role in controlling expression of cocaine sensitization (Filip et al., 2004), the question arises if actions at 5-HT2 receptors were responsible for the effect of the higher dose of SCH 23390 used in the experiment by White et al. (1998).
Prefrontal cortex D1 modulation of the reinforcing properties of cocaine
2006, Brain ResearchCitation Excerpt :Differences in intra-PFC SCH 23390 dosing may account for this discrepancy as the concentrations (0.5–2.0 μg/side) were 2- to 8-fold greater than in the present study. It is notable that, in addition to binding to D1 receptors, SCH 23390 has been demonstrated to have a weak affinity for 5-HT1, 5-HT2 and α-adrenergic receptors (Bischoff et al., 1986, 1988; Hicks et al., 1984). Therefore, high doses of SCH 23390 increase both the impact on D1 receptors and the likelihood of immediate interactions with additional receptors.
Dopamine D2 receptor activation increases vesicular dopamine uptake and redistributes vesicular monoamine transporter-2 protein
2004, European Journal of PharmacologySomatodendritic dopamine release in rat substantia nigra influences motor performance on the accelerating rod
2003, Brain ResearchCitation Excerpt :A previous study by Timmerman and Abercrombie [46] reported that increases in motor activity evoked by nigral amphetamine injections could be blocked by co-injections of SCH 23390, indicating that D1/D5-receptors in SN can have a facilitating role for motor activity. In the literature, SCH 23390 concentrations of 1–100 μM are often used for reverse dialysis, and the results are interpreted as D1/D5-specific, but even though only a small fraction of the perfused substance reaches the tissue, the selectivity for D1/D5- over D2/D3-receptors can be questioned with this regime (see Ref. [26]) and SCH 23390 may, at 100 μM, even affect 5HT-receptors or potassium channels [20,28]. We can therefore not exclude that some motor impairment seen with 10 and 100 μM SCH 23390 is non-specific.
Intra-prefrontal cortex injections of SCH 23390 influence nucleus accumbens dopamine levels 24 h post-infusion
2001, Brain ResearchCitation Excerpt :Another potential explanation for finding that intra-mPFC D1 antagonist, but not the agonist, influenced NAcc DA levels is the possible binding of SCH 23390 with other receptors. In addition to binding to dopamine D1 receptors, SCH 23390 has been demonstrated to have a weak affinity for 5-HT1, 5-HT2 and α-adrenergic receptors [6,7,26]. One study suggests that intra-mPFC SCH 23390 exerts effects on the mesolimbic DA system independent of actions on 5-HT or adrenergic receptors.