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Titolo:
Glutamate signaling and the fetal alcohol syndrome
Autore:
Olney, JW; Wozniak, DF; Jevtovic-Todorovic, V; Ikonomidou, C;
Indirizzi:
Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA WashingtonUniv St Louis MO USA 63110 pt Psychiat, St Louis, MO 63110 USA Washington Univ, Sch Med, Dept Anesthesiol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Anesthesiol, St Louis, MO 63110 USA Humboldt Univ, Charite, Dept Pediat Neurol, Berlin, Germany Humboldt UnivBerlin Germany arite, Dept Pediat Neurol, Berlin, Germany
Titolo Testata:
MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS
fascicolo: 4, volume: 7, anno: 2001,
pagine: 267 - 275
SICI:
1080-4013(2001)7:4<267:GSATFA>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL-NERVOUS-SYSTEM; METHYL-D-ASPARTATE; DEVELOPING RAT-BRAIN; EXCITATORY AMINO-ACIDS; APOPTOTIC CELL-DEATH; HIPPOCAMPAL-NEURONS; NMDA ANTAGONISTS; ISCHEMIC DAMAGE; CAUTIONARY NOTE; HEAD TRAUMA;
Keywords:
NMDA receptors; GABA receptors; synaptogenesis; apoptosis; ethanol; phencyclidine; ketamine; barbiturates; benzodiazepines; anesthetics;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
81
Recensione:
Indirizzi per estratti:
Indirizzo: Olney, JW Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 t, St Louis, MO 63110 USA
Citazione:
J.W. Olney et al., "Glutamate signaling and the fetal alcohol syndrome", MENT RET D, 7(4), 2001, pp. 267-275

Abstract

It has been known for three decades that ethanol, the most widely abused drug in the world, has deleterious effects on the developing human brain, but progress has been slow in developing animal models that are optimal for studying this problem, and the underlying mechanisms have remained elusive. Recently, we have shown that during the synaptogenesis period, also known as the brain growth spurt period, ethanol has the potential to trigger widespread neuronal suicide (apoptosis), deleting many millions of neurons from the in vivo mammalian brain. It appears that ethanol triggers apoptotic neurodegeneration by a dual mechanism (blockade of NMDA glutamate receptors and excessive activation of GABA receptors), in that ethanol has both NMDA antagonist and GABAmimetic properties; we have shown that other drugs which have either of these properties trigger apoptotic neurodegeneration in the developing brain. The brain growth spurt period in humans spans the last trimester of pregnancy and the first several years after birth. Thus, our findings provide a likely explanation for the reduced brain mass and neurobehavioral disturbances associated with the human fetal alcohol syndrome. Furthermore, since NMDA antagonist and GABAmimetic drugs are sometimes abused by pregnant women and also are used as anticonvulsants, sedatives, or anesthetics in pediatric medicine, our findings suggest the possibility that exposure of the developing brain to these various drugs either pre or postnatallycould contribute to mental disability syndromes that have heretofore been attributed to unknown causes. In addition, the observation that ethanol andrelated drugs trigger massive neuronal apoptosis in the developing brain provides an unprecedented opportunity to study both neuropathological aspects and molecular mechanisms of apoptotic neurodegeneration in the in vivo mammalian brain. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 00:22:44