SCH 23390 hydrochloride - CAS 125941-87-9
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
Dopamine Receptor
SCH 23390 hydrochloride is the hydrochloride salt of SCH 23390 which is a dopamine receptor antagonist. SCH 23390, a halobenzazepine, is a selective antagonist of the dopamine D1-like receptor subtypes D1 (Kis = 0.2 nM) and D5 (Kis = 0.3 nM).
Brife Description:
A potent dopamine receptor D1 antagonist
SCH 23390 hydrochloride; SCH-23390 hydrochloride; SCH23390 hydrochloride; (5R)-8-chloro-3-methyl-5-phenyl-1,2,4,5-tetrahydro-3-benzazepin-7-ol;hydrochloride
DMSO: ≥ 32 mg/mL
Store in a cool and dry place (or refer to the Certificate of Analysis).
Canonical SMILES:
1.AF64A lesions of mouse striatum result in ipsilateral rotations to D2 dopamine agonists but contralateral rotations to muscarinic cholinergic agonists.
Zhou LW;Zhang SP;Connell TA;Weiss B J Pharmacol Exp Ther. 1993 Feb;264(2):824-30.
Behavioral and anatomical evidence supports an interaction between the dopaminergic and cholinergic systems in regulating certain behavioral conditions and motor functions. In this study, we utilized the cholinotoxin, acetylethylcholine mustard aziridinium ion (AF64A), to lesion the mouse corpus striatum in order to examine the role of cholinergic interneurons in striatum on cholinergic- and dopaminergic-mediated rotational behavior. Mice were unilaterally lesioned with AF64A and then challenged with a variety of dopaminergic and cholinergic agonists and antagonists. The results show that mice with AF64A-induced lesions rotate ipsilaterally to challenge doses of the dopamine agonists, apomorphine and pergolide, but rotate contralaterally to challenge injections of the cholinergic agonist, oxotremorine. The gamma aminobutyric acid (GABA) agonist, muscimol, and the M1 agonist, (4-hydroxy-2-butynyl)-1-trimethylammonium m-chlorocarbanilate chloride failed to elicit rotational behavior. The D1 dopamine receptor antagonist, R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl- 2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride, inhibited rotations induced by apomorphine at concentrations 10-fold lower than those needed to block the effects of pergolide.
2.Inhibition of monoamine oxidases desensitizes 5-HT1A autoreceptors and allows nicotine to induce a neurochemical and behavioral sensitization.
Lanteri C;Hernández Vallejo SJ;Salomon L;Doucet EL;Godeheu G;Torrens Y;Houades V;Tassin JP J Neurosci. 2009 Jan 28;29(4):987-97. doi: 10.1523/JNEUROSCI.3315-08.2009.
Although nicotine is generally considered to be the main compound responsible for addictive properties of tobacco, experimental data indicate that nicotine does not exhibit all the characteristics of other substances of abuse. We recently showed that a pretreatment with mixed irreversible monoamine oxidases inhibitors (MAOIs), such as tranylcypromine, triggers a locomotor response to nicotine in mice and allows maintenance of behavioral sensitization to nicotine in rats. Moreover, we showed by microdialysis in mice that behavioral sensitization induced by compounds belonging to main groups of drugs of abuse, such as amphetamine, cocaine, morphine, or alcohol, was underlain by sensitization of noradrenergic and serotonergic neurons. Here, this neurochemical sensitization was tested after nicotine, tranylcypromine, or a mixture of both compounds. Data indicate that, whereas neither repeated nicotine nor repeated tranylcypromine alone has any effect by itself, a repeated treatment with a mixture of nicotine and tranylcypromine induces both behavioral sensitization and sensitization of noradrenergic and serotonergic neurons. The development of neurochemical and behavioral sensitizations is blocked by prazosin and SR46349B [(1Z,2E)-1-(2-fluoro-phenyl)-3-(4-hydroxyphenyl)-prop-2-en-one-O-(2-dimethylamino-ethyl)-oxime hemifumarate], two antagonists of alpha1b-adrenergic and 5-HT(2A) receptors, respectively, but not by SCH23390 [R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride], a D(1) receptor antagonist.
3.Motivational effects mu- and kappa-opioid agonists following acute and chronic restraint stress: involvement of dopamine D(1) and D(2) receptors.
del Rosario Capriles N;Cancela LM Behav Brain Res. 2002 May 14;132(2):159-69.
The influence of both acute and chronic restraint stress on the rewarding properties of morphine (1, 2 or 3 mg/kg i.p.) and the aversive effects of naloxone (0.5 mg/kg i.p. x3 or 1.0 mg/kg i.p.) or bremazocine (0.4 mg/kg i.p.) was investigated. An acute (2 h) but not chronic restraint (2 h daily for 7 days) enhanced the morphine place preference, and elicited a place aversion with a subthreshold dose of bremazocine. This enhancing effect on the reinforcing properties induced by the drugs was prevented by either R(+)-SCH-23390 hydrochloride (R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H3-benzazepine, 30 microg/kg i.p.) or (+/-)-sulpiride (60 mg/kg i.p.), 10-20 min prior to the stress session. Naltrexone pretreatment (1 mg/kg i.p.) abolished the stress effect on morphine place preference but not that on bremazocine aversion. Instead, nor-BNI (30 microg/3 microl i.c.v.) abolished the stress's effects on bremazocine aversion, but did not modify those on morphine preference. These results show that: (1) acute stress enhanced the morphine and bremazocine conditioned reinforcing effects meanwhile chronic stress did not modify them; (2) the stimulation of D(1) and D(2) dopamine receptors is necessary for the development of restraint stress-induced sensitization to the conditioned reinforcing effects of drugs; and (3) the stimulation mu/delta- and kappa-opioid receptors seems to be differentially involved.
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CAS 125941-87-9 SCH 23390 hydrochloride

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