Introduction: Amisulpride appears to be an effective atypical agent for treating schizophrenia in a dose-dependent manner.
Methods: 29 patients suffering from schizophrenia or schizoaffective disorder were treated with a broad dose range of amisulpride (50-1 200 mg/day, mean: 455.2+/-278.8 mg/day). After 2 weeks, brain single photon emission tomography (SPET) scans were performed two hours after intravenous injection of 185 MBq [123I]IBZM. Clinical evaluations and ratings of extrapyramidal symptoms were performed at baseline and after steady state treatment of two weeks with amisulpride.
Results: In patients treated with amisulpride, specific binding of [123I]IBZM to D2 receptors was significantly decreased (p<0.001) compared to healthy controls. D2 receptor blockade correlated well with administered doses and plasma concentrations of amisulpride. Extrapyramidal side effects, which had to be treated with biperiden, were observed in 31% of the patients. Clinical response was very good, without correlation between the response and striatal D2 occupancy.
Discussion: Within the first two weeks of treatment with the atypical antipsychotic amisulpride a significant occupancy of striatal postsynaptic dopamine D2 receptors was achieved. At the same time amisulpride shows an excellent tolerability with good efficacy.
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http://dx.doi.org/10.1055/s-2008-1076727 | DOI Listing |
Nat Ment Health
April 2024
Wellcome Centre for Human Neuroimaging, University College London, London, UK.
Striatal dopamine is important in paranoid attributions, although its computational role in social inference remains elusive. We employed a simple game-theoretic paradigm and computational model of intentional attributions to investigate the effects of dopamine D2/D3 antagonism on ongoing mental state inference following social outcomes. Haloperidol, compared with the placebo, enhanced the impact of partner behaviour on beliefs about the harmful intent of partners, and increased learning from recent encounters.
View Article and Find Full Text PDFOrphanet J Rare Dis
December 2023
Institute of Genomic Medicine and Rare Disorders, Semmelweis University Budapest, Budapest, Hungary.
Background: Huntington's disease (HD) is a progressive neurodegenerative disease, characterised by motor disturbances and non-motor (i.e., psychiatric) symptoms.
View Article and Find Full Text PDFbioRxiv
September 2023
National Institute on Drug Abuse Intramural Research Program, 251 Bayview Boulevard, Baltimore, MD 21224, USA.
Chronic psychostimulant use can cause long lasting changes to neural and cognitive function that persist even after long periods of abstinence. As cocaine users transition from drug use to abstinence, a parallel transition from hyperactivity to hypoactivity has been found in orbitofrontal-striatal glucose metabolism, and striatal D2/D3 receptor activity. Targeting these changes pharmacologically, using highly selective dopamine D3 receptor (DR) antagonists and partial agonists, has shown significant promise in reducing drug-taking, and attenuating relapse in animal models of cocaine and opioid use disorder.
View Article and Find Full Text PDFExp Neurol
November 2023
Department of Translational Neuroscience, College of Human Medicine, Michigan State University, 400 Monroe Ave. N.W., Grand Rapids, MI 49503, USA; Hauenstein Neuroscience Center, Mercy Health Saint Mary's, 220 Cherry St. S.E., Grand Rapids, MI 49503, USA.
Dopamine depletion associated with parkinsonism induces plastic changes in striatal medium spiny neurons (MSN) that are maladaptive and associated with the emergence of the negative side-effect of standard treatment: the abnormal involuntary movements termed levodopa-induced dyskinesia (LID). Prevention of MSN dendritic spine loss is hypothesized to diminish liability for LID in Parkinson's disease. Blockade of striatal CaV1.
View Article and Find Full Text PDFPsychiatry Res Neuroimaging
August 2023
Department of Psychology and Neuroscience, University of North Carolina-Chapel Hill, Chapel Hill, NC, United States; Department of Psychiatry, University of North Carolina-Chapel Hill, Chapel Hill, NC, United States; Carolina Institute for Developmental Disabilities, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, Chapel Hill, NC, United States.
Background: Anhedonia is hypothesized to be associated with blunted mesocorticolimbic dopamine (DA) functioning in samples with major depressive disorder. The purpose of this study was to examine linkages between striatal DA, reward circuitry functioning, anhedonia, and, in an exploratory fashion, self-reported stress, in a transdiagnostic anhedonic sample.
Methods: Participants with (n = 25) and without (n = 12) clinically impairing anhedonia completed a reward-processing task during simultaneous positron emission tomography and magnetic resonance (PET-MR) imaging with [C]raclopride, a DA D2/D3 receptor antagonist that selectively binds to striatal DA receptors.
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