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http://dx.doi.org/10.1111/pcn.13705 | DOI Listing |
Psychiatry Clin Neurosci
September 2024
Champalimaud Research and Clinical Centre, Champalimaud Centre for the Unknown, Lisbon, Portugal.
Neuropsychiatr Dis Treat
March 2016
Department of Neurology, Anna Gostynska Wolski Hospital, Medical University of Warsaw, Warsaw, Poland; Department of Neurology, Faculty of Health Sciences, Medical University of Warsaw, Warsaw, Poland.
Tetrabenazine is used in the treatment of chorea, tardive dyskinesia, tics, and dystonia. It rarely causes acute eyeball dystonia and the description of this complication in Gilles de la Tourette syndrome is limited. We provide a description of an acute oculogyric crisis caused by tetrabenazine in a patient with severe tics.
View Article and Find Full Text PDFBioorg Med Chem
May 2001
Research Institute, Fujimoto Pharmaceutical Corporation, Matsubara, Osaka 580-8503, Japan.
The catecholaminergic and serotoninergic neurons in the brain change their performance according to the physiological need via a catecholaminergic/serotoninergic activity enhancer (CAE/SAE) mechanism. Phenylethylamine (PEA), tyramine and tryptamine are the presently known endogenous CAE/SAE substances which enhance the impulse propagation mediated release of catecholamines and serotonin in the brain. A PEA derivative, (-)deprenyl (selegiline), known as a selective inhibitor of MAO-B, is for the time being the only CAE/SAE substance in clinical use.
View Article and Find Full Text PDFBr J Pharmacol
December 1999
Department of Pharmacology, Semmelweis University of Medicine, P.O.B. 370, H-1445, Hungary.
1. The brain constituents beta-phenylethylamine (PEA) and tryptamine enhance the impulse propagation mediated transmitter release (exocytosis) from the catecholaminergic and serotoninergic neurons in the brain ('catecholaminergic/serotoninergic activity enhancer, CAE/SAE, effect'). (-)Deprenyl (Selegiline) and (-)1-phenyl-2-propylaminopentane [(-)PPAP] are amphetamine derived CAE substances devoid of the catecholamine releasing property.
View Article and Find Full Text PDFIt has been suggested that the neuroleptic-induced acute dyskinetic syndrome in monkeys may be a useful model of extrapyramidal dysfunction. Various drugs that have well-characterized effects on clinical extrapyramidal syndromes and on catecholaminergic, cholinergic, or GABAergic neurotransmission were assessed in dyskinesia-susceptible squirrel monkeys. Catecholamine depletors (alpha-methyl-p-tyrosine, tetrabenazine) induced the syndrome, as do dopamine (DA) receptor antagonists, and d-amphetamine reversed the effects of tetrabenazine.
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