Disease relevance of SCH-23390

• Haloperidol- but not SCH 23390-induced catalepsy was attenuated by intrastriatally administered 7-chlorokynurenate [1].
• Administration of the D1 antagonist SCH-23390 1 hour before administration of (+)-PHNO did not change the dyskinesia [2].
• However, a rebound exaggeration of chorea was observed following SCH 23390 at the time when chorea induced by L-dopa alone would normally be subsiding [3].
• In contrast, PD 128907-induced hypothermia was antagonized by SCH 23390, a selective D(1) receptor antagonist, and by L-741,626, a selective D(2) receptor antagonist [4].
• The initial phase was enhanced by SCH 23390 and converted to a transient hypotension by idazoxan [5].

Psychiatry related information on SCH-23390

• In contrast, full retrograde amnesia was obtained when SCH 23390 (0.5 microg/side), a D1/D5 receptor antagonist, was infused into the hippocampus 3 or 6 h after training [6].
• This was assessed by studying how retrodialysis application of NMDA (50 mM, 10 min) affects motor activity and NAc DA levels during simultaneous retrodialysis administration of the D1/D5 receptor antagonist SCH 23390 (100 and 250 microM, 60 min) or the D2 receptor antagonist raclopride (100 and 250 microM, 60 min) [7].
• SCH 23390 (0.1 to 2.0 mg/kg) increased slow-wave sleep (SWS), whereas wakefulness (W) and REMS were decreased [8].
• Over a very small dose range (0.003-0.03 mg/kg, subcutaneously), SCH 23390 significantly increased the time spent in total sleep, including rapid eye movement (REM) and non-REM sleep [9].
• A comparison of the effects of the D1 receptor antagonists SCH 23390 and SCH 39166 on suppression of feeding behavior by the D1 agonist SKF38393 [10].

High impact information on SCH-23390

• Pretreatment with intraperitoneal injection of 20 microgram/kg SCH 23390, a D1 receptor antagonist, reversed the SKF 81297 response [11].
• Apomorphine increased sensory stimulation-evoked gene expression in the barrel cortex, and intrastriatal infusion of SCH-23390 attenuated this effect [12].
• Regression analysis showed that estimates of CFT k3/k4 were positively correlated with those of SCH 23390 k3/k4 in the striatum in normal control, whereas the two binding estimates were less positively correlated in the caudate and inversely correlated in the putamen in PD [13].
• In some animals, D1 (SCH 23390) or D2 (pimozide) receptor antagonists were injected systemically prior to or during self-administration sessions to assess the effects of dopamine receptor blockade on anticipatory and postcocaine responses [14].
• The D1 and D2 receptor binding sites were labeled with the selective high-affinity antagonists SCH 23390 and N-(p-aminophenethyl)-spiperone (NAPS), respectively, coupled to either Bodipy or Texas red fluorophores [15].

Chemical compound and disease context of SCH-23390

• The D1 dopamine receptor antagonist SCH 23390 enhances REM sleep in the rat [9].
• (The sulpiride/SCH 23390 treatment protects DA receptors from EEDQ-induced inactivation.) NPA's (0.1 or 1.0 mg/kg) effects on locomotor activity and grooming were assessed 1, 2, 4 and 8 days after the EEDQ pretreatment [16].
• However, the ability of both SKF 38393 and SCH 23390 to inhibit quinpirole locomotor activity suggests some interaction between D-1 and D-2 systems to occur in this species [17].
• Moreover, co-administration of YM-09151 with SCH 23390 produced a marked increase in the incidence of catalepsy [18].
• 2. IL-8 evoked a dose-dependent hyperalgesia which was attenuated by a specific antiserum, the beta-adrenoceptor antagonists atenolol and propranolol, the dopamine receptor antagonist SCH 23390 and the adrenergic neurone-blocking agent guanethidine [19].

Biological context of SCH-23390

• Intravenous (i.v.) infusions of SCH 23390 (R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7- ol) produced dose-related antagonism of dopamine (DA)-induced renal vasodilation in phenoxybenzamine-treated dogs at infusion rates of 0.05, 0.15, and 0.5 microgram/kg/min [20].
• Intrarenal arterial infusion of the dopamine-1 antagonist SCH-23390 alone induced an antinatriuresis, without affecting glomerular filtration rate, in normotensive but not in hypertensive rats [21].
• At the infusion rates used in these studies, SCH 23390 did not affect arterial blood pressure or heart rate [20].
• When the D-1 receptor blocker SCH 23390 was added to the incubation medium, DA elicited a dose-dependent inhibition of adenylate cyclase (IC50, 10 microM); (-)sulpiride specifically blocked this effect [22].
• DA-mediated up-regulation of HO-1 was not influenced by the addition of either the D2-receptor antagonist haloperidol or the D1-receptor antagonist SCH 23390 [23].

Anatomical context of SCH-23390

• Net production of cerebrospinal fluid is decreased by SCH-23390 [24].
• Experiments using SCH 23390 suggest that the reinforcing effects of food, water, saccharin, heroin and brain stimulation all critically depend on the activation of D1 dopamine receptors, particularly those in the nucleus accumbens and the ventral tegmental area [25].
• The D1 receptor identified here appears to be the one responsible for the physiological effects on the parathyroid gland, because dopamine-stimulated cAMP accumulation is stereoselectively blocked by the D1 receptor antagonist SCH-23390 in dispersed cells of the parathyroid gland [26].
• We found that 14-day treatment with SCH-23390 (1.0 mg/kg per day) or haloperidol (0.5 mg/kg per day) caused an increase in the percentage of perforated synapses within the caudate but not the nucleus accumbens [27].
• However, perfusion of the substantia nigra with a lower concentration of quinpirole (1 microM) and the D1 antagonist SCH 23390 (10 microM) did not affect the nigral L-DOPA biotransformation [28].

Associations of SCH-23390 with other chemical compounds

• Iodinated SCH 23390, 125I-SCH 23982 (DuPont-NEN), was examined using quantitative autoradiography for its potency, selectivity, and anatomical and neuronal localization of binding to the dopamine D1 receptor in rat brain sections [29].
• Both the contraversive rotation and the induction of Fos-like immunoreactivity were blocked by the preadministration of the D1-preferring antagonist SCH-23390 and the D2-selective antagonist raclopride in combination [30].
• Unilateral injections of SCH-23390 into the PFC in the hemisphere contralateral to a microinjection of lidocaine into the hippocampus severely disrupted performance of the delayed task [31].
• 4. Drugs acting at 5-HT1, 5-HT2, alpha- and beta-adrenergic, dopaminergic, and histaminergic receptors (methysergide, ketanserin, propranolol, phentolamine, sulpiride, SCH 23390, cimetidine) were essentially inactive at 10 mumol/liter [32].
• In cultured GC, DA and SKF-38393 induced increased threonine-phosphorylation of DARPP-32, even in the presence of propranolol but not in the presence of D1-R antagonist SCH-23390 [33].

Gene context of SCH-23390

• Selective stimulation of D1 receptors with the agonist SKF R-38393 caused p-ERK1/2, but not p-JNK or p-p38 MAPK activation, in a manner sensitive to the receptor-selective antagonist SCH 23390, protein kinase A inhibition (KT5720), and MEK1/2 inhibition (U0126 or PD98059) [34].
• Furthermore, THC-induced phosphorylation of the transcription factor Elk-1, and up-regulation of zif268 mRNA expression are blocked by SL327, a specific inhibitor of MAPK/ERK kinase (MEK), the upstream kinase of ERK, as well as SCH 23390 [35].
• The D(5) receptor agonist fenoldopam decreases PLD2, but not PLD1, expression and activity in human embryonic kidney-293 cells heterologously expressing the human D(5) receptor, effects that are blocked by the D(5) receptor antagonist SCH-23390 [36].
• Pretreatment with the D1 antagonist SCH-23390 ((R)-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7-OL maleate) inhibited the prolonged increase in MPC phospho-ERK, whereas the 5-HT2 receptor antagonist ketanserin (3-[2-[4-(4-fluorobenzoyl)-1-piperidinyl]ethyl]-2,4(1H,3H)-quinazolinedione tartrate) was ineffective [37].
• Interestingly, catalepsy induced by raclopride, a specific dopamine D(2)/D(3) antagonist is completely abolished in NGFI-B-deficient mice whereas the cataleptic response to SCH 23390, a dopamine D(1) agonist, is preserved [38].

Analytical, diagnostic and therapeutic context of SCH-23390

• In situ hybridization showed that LEK-8829 induced the expression of neurotensin and ania-4 mRNAs in dopamine-intact striatum that could be completely blocked only by the combined treatment with SCH-23390 and quinpirole [39].
• Microdialysis probes were implanted in both striata, and a D1 antagonist (SCH-23390, 100 microM) was administered through one probe and modified Ringer's solution through the other [40].
• Since these two phenomena are causally linked, the alterations in the tubuloglomerular feedback response by the luminal application of dopamine, the D1 agonist fenoldopam, the D2 agonist bromocriptine and the D1 and D2 antagonists SCH 23390 and metoclopramide were further investigated using the micropuncture technique [41].
• The D1 antagonist, SCH 23390, by itself (0.03-0.3 mg/kg i.v.) produced small changes in the EEG and no evidence of sedation [42].
• When PLG (1.0 mg/kg/d.i.p.) was administered together with SCH 23390 for the initial 32 days from birth, the binding of [3H]SCH 23390 to homogenates of the striatum was unchanged from that of the control group at 8 weeks [43].

References