SCH 23390

06/13/1996 - "A significant reduction in [3H] SCH23390 binding was found in the striatum from 48 h after ischemia. "
11/01/1992 - "The ventromedial striatum and dentate gyrus which were resistant to ischemia also exhibited a significant reduction in [3H]SCH 23390 binding. "
09/15/2004 - "These results suggest that [3H]-SCH23390 and [3H]-NMPB binding do not correlate with cell injury by ischemia/reperfusion, although vulnerability to ischemia/reperfusion was observed with these receptors. "
09/15/2004 - "[3H]-SCH23390 binding was reduced to 47% of the contralateral side at 3 days after ischemia/reperfusion of MCA. "
08/02/1993 - "Furthermore, this drug significantly prevented postischemic reduction in [3H]SCH 23390 binding (only) 7 days after ischemia. "

01/01/1990 - "SCH 23390 did not alter the incidence of stimulant-induced seizures compared to the vehicle controls. "
01/01/2001 - "SCH 23390 affords protection against soman-evoked seizures in the freely moving guinea-pig: a concomitant neurochemical, electrophysiological and behavioural study."
01/01/2011 - "Electrophysiological recordings in the dentate gyrus revealed the presence of epileptiform discharges peaking at 30-45 min post-injection and declining by 60 min. Seizures were prevented by the D1-type receptor antagonist, SCH 23390, or the cannabinoid CB1 receptor agonist, CP 55,940. "
02/23/2004 - "The dopamine D1-like receptor antagonist SCH 23390 [R(+)-3-methyl-7-chloro-8-hydroxy-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine] readily antagonised these responses to SK&F 83822, particularly seizure activity. "
01/01/2001 - "We found that the blockade of the D(1) receptor with SCH 23390 can inhibit seizure activity, while blockade of the D(2) receptor with sulpiride can augment the evoked seizure activity. "

06/01/1987 - "In combination studies, the D2 blockers reversed the effects of stimulation of D2 receptors and released normal behaviour, whereas SCH 23390 converted both the behavioural syndromes mediated by pre- and postsynaptic D2-receptors into severe inactivity (but not catalepsy). "
04/01/2014 - "The effects of PDE10A inhibition against dopaminergic stimulants and on catalepsy were potentiated by the D(1) antagonist SCH-23390 (8-chloro-3-methyl-5-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepin-7-ol), suggesting that enhancement of D(1) receptor-mediated neurotransmission contributes to the behavioral profile of PDE10AIs. "
11/01/2012 - "Significant catalepsy sensitization was not observed in rats repeatedly tested with SCH 23390. "
01/01/2000 - "Basal catalepsy was increased and SCH23390 was unable to further enhance catalepsy beyond the basal levels in the lesioned animals. "
05/01/1998 - "2. A challenge dose of SCH23390 exhibited enhanced catalepsy when given 15 days, but not at 24 h, after the last pretreatment dose of SCH23390 (0.1-1.0 mg/kg s.c.). "

02/01/1998 - "SCH-23390 eliminated L-dopa induced self-mutilation in all subjects, while risperidone eliminated self-mutilation in all but one subject."
02/01/1990 - "SCH-12679 antagonized the self-mutilation behavior and behavioral responses induced by L-dihydroxyphenylalanine in neonatal-6-OHDA lesioned rats in a manner similar to the prototypic D1-dopamine antagonist SCH-23390 and, like SCH-23390, produced a deficit in avoidance responding in unlesioned rats. "

07/01/2003 - "Maternal administration of a D1 dopamine antagonist, SCH 23390, before either cocaine or asphyxia exposure dramatically reduced the numbers of Fos-immunoreactive cells in the striatum as well as in many other brain regions. "
07/01/1997 - "Perinatal asphyxia reduced D1 antagonist binding ([3H]SCH 23390 in the presence of ketanserine) in the accumbens nucleus, the olfactory tubercle, and the substantia nigra and increased D1 agonist binding ([3H]dopamine in the presence of spiperone) in the accumbens nucleus and the olfactory tubercle. "