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Titolo:
Environmental agents that have the potential to trigger massive apoptotic neurodegeneration in the developing brain
Autore:
Olney, JW; Farber, NB; 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, Dept Pediat Neurol, Berlin, Germany Humboldt Univ Berlin Germany Univ, Dept Pediat Neurol, Berlin, Germany
Titolo Testata:
ENVIRONMENTAL HEALTH PERSPECTIVES
, volume: 108, anno: 2000, supplemento:, 3
pagine: 383 - 388
SICI:
0091-6765(200006)108:<383:EATHTP>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
NMDA-ANTAGONIST NEUROTOXICITY; CORTICAL ACETYLCHOLINE-RELEASE; IN-VIVO MICRODIALYSIS; DEVELOPING RAT-BRAIN; CELL-DEATH; MK-801 NEUROTOXICITY; CAUTIONARY NOTE; NITROUS-OXIDE; AMINO-ACIDS; PHENCYCLIDINE;
Keywords:
anesthetics; apoptosis; barbiturates; benzodiazepines; ethanol; GABA(A) receptors; ketamine; NMDA receptors; phencyclidine; synaptogenesis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Olney, JW Washington Univ, Sch Med, Dept Psychiat, Campus Box 8134,660 S Euclid, St Louis, MO 63110 USA Washington Univ Campus Box 8134,660 S Euclid St Louis MO USA 63110
Citazione:
J.W. Olney et al., "Environmental agents that have the potential to trigger massive apoptotic neurodegeneration in the developing brain", ENVIR H PER, 108, 2000, pp. 383-388

Abstract

We review recent findings pertaining to several environmental agents (ethanol, phencyclidine, ketamine, nitrous oxide, barbiturates, benzodiazepines,halothane, isoflurane, and propofol) that have the potential to delete large numbers of neurons from the developing brain by a newly discovered mechanism involving interference in the action of neurotransmitters [glutamate and gamma-amino butyric acid (GABA at N-methyl-D-aspartate (NMDA)I and GABA(A) receptors during the synaptogenesis period, also known as the brain growth-spurt period. Transient interference (lasting greater than or equal to 4hr) in the activity of these transmitters during the synaptogenesis period(the last trimester of pregnancy and the first several years after birth in humans) causes millions of developing neurons to commit suicide idle by apoptosis). Many of these agents are drugs of abuse (ethanol is a prime example) to which the human fetal brain may be exposed during the third trimester by drug-abusing mothers. Ethanol triggers massive apoptotic neurodegeneration in the developing brain by interfering with both the NMDA and GABA(A)receptor systems, and this can explain the reduced brain mass and lifelongneurobehavioral disturbances associated with intrauterine exposure of the human fetus to ethanol (fetal alcohol syndrome). Exposure of the immature brain in a medical treatment context is also of concern because many of these agents are drugs used frequently as sedatives, tranquilizers, anticonvulsants, or anesthetics in pediatric and/or obstetrical medicine. Because thisis a newly discovered mechanism, further research will be required to fully ascertain the nature and degree of risk posed by exposure of the developing human brain to environmental agents that act by this mechanism.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 12:05:00