Neurotransmitters and apoptosis in the developing brain

Citation
C. Ikonomidou et al., Neurotransmitters and apoptosis in the developing brain, BIOCH PHARM, 62(4), 2001, pp. 401-405
Citations number
35
Language
INGLESE
art.tipo
Editorial Material
Categorie Soggetti
Pharmacology & Toxicology
Journal title
BIOCHEMICAL PHARMACOLOGY
ISSN journal
0006-2952 → ACNP
Volume
62
Issue
4
Year of publication
2001
Pages
401 - 405
Database
ISI
SICI code
0006-2952(20010815)62:4<401:NAAITD>2.0.ZU;2-F
Abstract
In the immature mammalian brain during a period of rapid growth (brain grow th spurt/synaptogenesis period), neuronal apoptosis can be triggered by the transient blockade of glutamate N-methyl-d-aspartate (NMDA) receptors, or the excessive activation of gamma -aminobutyric acid (GABA(A)) receptors. A poptogenic agents include anesthetics (ketamine, nitrous oxide, isoflurane, propofol, halothane), anticonvulsants (benzodiazepines, barbiturates), and drugs of abuse (phencyclidine, ketamine, ethanol). In humans, the brain gr owth spurt period starts in the sixth month of pregnancy and extends to the third year after birth. Ethanol, which has both NMDA antagonist and GABA(A ) agonist properties, is particularly effective in triggering widespread ap optotic neurodegeneration during this vulnerable period. Thus, maternal ing estion of ethanol during the third trimester of pregnancy can readily expla in the dysmorphogenic changes in the fetal brain and consequent neurobehavi oral disturbances that characterize the human fetal alcohol syndrome. In ad dition, there is basis for concern that agents used in pediatric and obstet rical medicine for purposes of sedation, anesthesia, and seizure management may cause apoptotic neuronal death in the developing human brain. (C) 2001 Elsevier Science Inc. All rights reserved.