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Titolo:
Blunted brain metabolic response to ketamine in mice lacking D-1A dopaminereceptors
Autore:
Miyamoto, S; Mailman, RB; Lieberman, JA; Duncan, GE;
Indirizzi:
Univ N Carolina, Sch Med, Dept Psychiat, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 chiat, Chapel Hill, NC 27599 USA Univ N Carolina, Sch Med, Dept Pharmacol, Chapel Hill, NC 27599 USA Univ NCarolina Chapel Hill NC USA 27599 macol, Chapel Hill, NC 27599 USA Univ N Carolina, Sch Med, Ctr Neurosci, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 rosci, Chapel Hill, NC 27599 USA Univ N Carolina, Sch Med, Mental Hlth & Neurosci Clin Res Ctr, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 s Ctr, Chapel Hill, NC 27599 USA
Titolo Testata:
BRAIN RESEARCH
fascicolo: 2, volume: 894, anno: 2001,
pagine: 167 - 180
SICI:
0006-8993(20010316)894:2<167:BBMRTK>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
CEREBRAL GLUCOSE-UTILIZATION; EMISSION-TOMOGRAPHY PET; PREFRONTAL CORTEX; RAT-BRAIN; LOCOMOTOR-ACTIVITY; HEALTHY-VOLUNTEERS; STRIATAL DOPAMINE; D1 RECEPTORS; NEUROMODULATORY ACTIONS; NUCLEUS-ACCUMBENS;
Keywords:
ketamine; D-1-like dopamine receptor; schizophrenia; N-methyl-D-aspartate antagonist; SCH23390; D-1A knockout mice;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
91
Recensione:
Indirizzi per estratti:
Indirizzo: Miyamoto, S Univ N Carolina, Sch Med, Dept Psychiat, CB 7090, Chapel Hill,NC 27599 USA Univ N Carolina CB 7090 Chapel Hill NC USA 27599 NC 27599 USA
Citazione:
S. Miyamoto et al., "Blunted brain metabolic response to ketamine in mice lacking D-1A dopaminereceptors", BRAIN RES, 894(2), 2001, pp. 167-180

Abstract

The interaction of glutamatergic and dopamine neurotransmission is thoughtto have relevance to both the pathophysiology and pharmacotherapy of schizophrenia. For example, subanesthetic doses of the N-methyl-D-aspartate receptor (NMDA-R) antagonist ketamine induce schizophrenia-like behavioral effects in humans and both behavioral and brain metabolic activation in rodents. Blockade of NMDA-R results in dopamine release, and antipsychotic drugs that block dopamine neurotransmission decrease NMDA-R antagonist-induced behavioral activation. The involvement of dopamine receptors in brain metabolic activation induced by ketamine is, however, unknown. The present study used D-1A knockout mice to determine the role of dopamine D-1A receptors in the effects of subanesthetic doses of ketamine on both behavioral responses and on alterations in regional [C-14]2-deoxyglucose (2-DG) uptake. There was less ketamine-induced behavioral activation in D-1A knockout mice than inwild-type mice. In wild-type mice, ketamine (30 mg/kg) induced dramatic increases in 2-DG uptake in limbic cortical regions, hippocampal formation, nucleus accumbens, basolateral amygdala, and caudal parts of the substantia nigra pars reticulata. D-1A knockout mice exhibited blunted metabolic activation in response to ketamine in a neuroanatomically specific manner. The selective D-1A antagonist, SCH23390 (0.3 mg/kg), inhibited both ketamine-induced brain metabolic activation and behavioral responses in the wild-type mice, with a similar neuroanatomical specificity observed in the D-1A knockout mice. Thus, the neuroanatomically selective role that D-1A receptors play in ketamine-induced behavior and regional brain metabolic activation in mice provides a useful model for further studies of how the D-1A receptor function may be altered in schizophrenia. (C) 2001 Elsevier Science B.V. All rights reserved.

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Documento generato il 19/01/20 alle ore 20:11:05