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Titolo:
Effects of (S)-ketamine on striatal dopamine: a [C-11]raclopride PET studyof a model psychosis in humans
Autore:
Vollenweider, FX; Vontobel, P; Oye, I; Hell, D; Leenders, KL;
Indirizzi:
Psychiat Univ Hosp Zurich, Res Dept, CH-8029 Zurich, Switzerland Psychiat Univ Hosp Zurich Zurich Switzerland CH-8029 Zurich, Switzerland Paul Scherrer Inst, PET Dept, CH-5232 Villigen, Switzerland Paul Scherrer Inst Villigen Switzerland CH-5232 32 Villigen, Switzerland Univ Oslo, Sch Med, Dept Pharmacol, N-0316 Oslo, Norway Univ Oslo Oslo Norway N-0316 ch Med, Dept Pharmacol, N-0316 Oslo, Norway
Titolo Testata:
JOURNAL OF PSYCHIATRIC RESEARCH
fascicolo: 1, volume: 34, anno: 2000,
pagine: 35 - 43
SICI:
0022-3956(200001/02)34:1<35:EO(OSD>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
METHYL-D-ASPARTATE; POSITRON-EMISSION-TOMOGRAPHY; PREFRONTAL CORTEX; SCHIZOPHRENIC-PATIENTS; HEALTHY-VOLUNTEERS; IN-VIVO; TRANSMITTER RELEASE; COMPETITIVE NMDA; CEREBRAL-CORTEX; C-11 RACLOPRIDE;
Keywords:
(S)-ketamine; NMDA receptor antagonist; glutamate; dopamine; striatum; psychopathology; human; schizophrenia; positron emission tomography (PET); dopamine D2 receptor; [C-11]raclopride;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Social & Behavioral Sciences
Clinical Medicine
Life Sciences
Citazioni:
57
Recensione:
Indirizzi per estratti:
Indirizzo: Vollenweider, FX Psychiat Univ Hosp Zurich, Res Dept, Box 68, CH-8029 Zurich, Switzerland Psychiat Univ Hosp Zurich Box 68 Zurich Switzerland CH-8029
Citazione:
F.X. Vollenweider et al., "Effects of (S)-ketamine on striatal dopamine: a [C-11]raclopride PET studyof a model psychosis in humans", J PSYCH RES, 34(1), 2000, pp. 35-43

Abstract

Administration of the N-methyl-D-aspartate (NMDA) antagonist S-ketamine innormals produces a psychosis-like syndrome including several positive and negative symptoms of schizophrenic disorders (Abi-Saab WM, D'Souza DC, Moghaddam B, Krystal JH. The NMDA antagonist model for schizophrenia: promise and pitfalls. Pharmacopsychiatry 1995;31:104-109). Given the clinical efficacy of dopamine (DA) D2 receptor antagonists in the treatment of positive symptoms, it is conceivable that S-ketamine-induced psychotic symptoms are partially due to a secondary activation of dopaminergic systems. To date, animal and human studies of the effects of NMDA antagonists on striatal DA levels have been inconsistent. The present study used positron emission tomography (PET) to determine whether a psychotomimetic dose of S-ketamine decreases the in vive binding of [C-11]raclopride to striatal DA D2 receptors in humans (n = 8). S-ketamine elicited a psychosis-like syndrome, including alterations in mood, cognitive disturbances, hallucinations and ego-disorders. S-ketamine decreased [C-11]raclopride binding potential (BP) significantly in the ventral striatum (-17.5%) followed by the caudate nucleus (-14.3%)and putamen (-13.6%), indicating an increase in striatal DA concentration. The change in raclopride BP in the ventral striatum correlated with heightened mood ranging from euphoria to grandiosity. These results provide evidence that the glutamatergic NMDA receptor may contribute to psychotic symptom formation via modulation of the DA system. (C) 2000 Elsevier Science Ltd. All rights reserved.

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Documento generato il 22/01/20 alle ore 07:23:58