Raclopride

12/01/2010 - "We found that systemic injection of raclopride given before extinction impaired retrieval of extinction when rats were tested drug-free the next day but also induced catalepsy during extinction training. "
07/01/2000 - "Raclopride (2 mg/kg) produced on average 95% and 87% D2 receptor occupancy 1 and 2 h after administration, respectively, and maximum catalepsy. "
07/01/2000 - "Raclopride (0.5-2 mg/kg) produced 83-95% D2 occupancy and significant catalepsy. "
07/01/2000 - "Using [3H]-raclopride, cold raclopride (0.01-0.2 mg/kg) produced 16-77% D2 receptor occupancy and no catalepsy. "
03/01/2000 - "phasic responsivity, in mesocortically projecting DA neurons, and also potentiate the CAR suppressant effect of the selective D(2)/D(3)-receptor antagonist raclopride without increasing catalepsy scores. "

01/01/1989 - "Efficacy, safety and tolerability of raclopride, a specific D2 receptor blocker, in acute schizophrenia: an open trial."
01/01/1988 - "An open label trial of raclopride in acute schizophrenia. "
09/01/2008 - "Eleven unaffected relatives from families with two or more first- or second-degree relatives with schizophrenia (n = 9) or with a monozygotic schizophrenic twin (n = 2) and 11 age- and sex-matched controls were examined using positron emission tomography (PET) with [(11)C] raclopride. "
11/15/2003 - "These sensorimotor gating deficits and neurochemical (greater AMPH-induced displacement of radio-raclopride binding) abnormalities show similarities with the pathophysiology of schizophrenia and suggest that the AMPH-sensitized-state rats could be used to model certain aspects of schizophrenia."
06/01/1997 - "The density of [3H]raclopride binding to tissue from subjects with schizophrenia was increased, unchanged or decreased depending on the methodology used. "

05/01/2013 - "In HC, [11C]raclopride binding in dorsal striatum correlated inversely with subjective effects of gambling (r = -0.70, P = 0.03) and impulsiveness (r = -0.70, P = 0.03). "
01/01/2013 - "Using [(11)C]raclopride with positron emission tomography, we assessed dopaminergic neurotransmission during Iowa Gambling Task performance. "
01/01/2013 - "We noted a marked decrease in [(11)C]raclopride binding in the left ventral striatum upon gambling, indicating a gambling-induced dopamine release. "
05/01/2013 - "The D2/3 dopamine receptor in pathological gambling: a positron emission tomography study with [11C]-(+)-propyl-hexahydro-naphtho-oxazin and [11C]raclopride."
05/01/2009 - "Increased striatal dopamine release in Parkinsonian patients with pathological gambling: a [11C] raclopride PET study."

04/10/2009 - "Both CGS21680 and raclopride significantly increased joint stiffness, the velocity independent component of rigidity that is most affected in Parkinsonism. "
09/01/2001 - "This review summarizes: (1) the PET scan findings (fluorodopa uptake and raclopride binding) in both familial parkinsonian syndromes and IP; and (2) the similarities and differences of the clinical and PET features between familial parkinsonian syndromes and IP. "
01/01/2001 - "Among the compounds investigated, including parkinsonism-inducing TIQ and (R/S)-1-benzyl-TIQ, parkinsonism-preventing (R)- and (S)-1-methyl-TIQ, and probable N-methylated metabolites of TIQ and 1-methyl-TIQ, TIQ and (S)-1-methyl-TIQ had the strongest effect on the binding of [11C]raclopride, and N-methylated derivatives showed less of an effect than the respective parent compounds. "
03/01/1995 - "Three patients with tremor and parkinsonism had their striatal [18F]-fluorodopa uptake and raclopride binding measured with positron emission tomography. "
02/23/1993 - "The high dose of raclopride is metabolically active in all brain areas, and, therefore, in clinical application might produce involuntary motor syndromes, like parkinsonism and late onset dyskinesias, along with its antipsychotic effects."

04/01/1994 - "Furthermore, raclopride-induced acute dyskinesia worsened during chronic treatment. "
02/23/1993 - "The high dose of raclopride is metabolically active in all brain areas, and, therefore, in clinical application might produce involuntary motor syndromes, like parkinsonism and late onset dyskinesias, along with its antipsychotic effects."
04/01/1994 - "Concomitant treatment with NNC 756 tended to reduce the D1 agonist SKF 81297-induced dyskinesia and grooming, while concomitant treatment with raclopride increased SKF 81297-induced dyskinesia and tended to decrease SKF 81297-induced grooming. "
04/01/1994 - "No significant dyskinesia was induced by NNC 756, while raclopride significantly induced both acute and tardive oral dyskinesia. "
07/28/1997 - "Pretreatment with (-)-OSU 6162 and raclopride, in doses increased by multiples of three, both dose-dependently relieved the levodopa-induced dyskinesias. "