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Triggers of apoptosis in the immature brain

Abstract Apoptosis occurs physiologically in the mammalian brain during the period of the growth spurt, which in human starts in the 3rd trimester of gestation and ends by the third year of life. Environmental factors can interact with programmed cell death mechanisms to increase the number of neuro...

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Published in:Brain & development (Tokyo. 1979) 2009-08, Vol.31 (7), p.488-492
Main Author: Ikonomidou, Chrysanthy
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Language:English
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description Abstract Apoptosis occurs physiologically in the mammalian brain during the period of the growth spurt, which in human starts in the 3rd trimester of gestation and ends by the third year of life. Environmental factors can interact with programmed cell death mechanisms to increase the number of neurons undergoing apoptosis and thus produce neuropathological sequelae in the brain. In a series of studies it could be shown that classes of drugs which block N-methyl- d -aspartate (NMDA) glutamate receptors, promote γ-aminobutyric-acid (GABAA ) receptor activation or block voltage gated sodium channels, when administered to immature rodents during the period of the brain growth spurt, trigger widespread apoptotic neurodegeneration throughout the developing brain. Studies have also shown that short exposures to non-physiologic oxygen levels can trigger apoptotic neurodegeneration in the brains of infant rodents. Pathomechanisms involved in the proapoptotic action of sedative and anticonvulsant drugs and oxygen include decreased expression of neurotrophins, inactivation of survival signaling proteins, activation of inflammatory cytokines as well as oxidative stress. These findings raise concerns pertaining to the treatment of infants and young children with sedative and anticonvulsant drugs and premature infants with oxygen. The experimental findings imply that new approaches should be developed for patients within these vulnerable age groups.
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Environmental factors can interact with programmed cell death mechanisms to increase the number of neurons undergoing apoptosis and thus produce neuropathological sequelae in the brain. In a series of studies it could be shown that classes of drugs which block N-methyl- d -aspartate (NMDA) glutamate receptors, promote γ-aminobutyric-acid (GABAA ) receptor activation or block voltage gated sodium channels, when administered to immature rodents during the period of the brain growth spurt, trigger widespread apoptotic neurodegeneration throughout the developing brain. Studies have also shown that short exposures to non-physiologic oxygen levels can trigger apoptotic neurodegeneration in the brains of infant rodents. Pathomechanisms involved in the proapoptotic action of sedative and anticonvulsant drugs and oxygen include decreased expression of neurotrophins, inactivation of survival signaling proteins, activation of inflammatory cytokines as well as oxidative stress. These findings raise concerns pertaining to the treatment of infants and young children with sedative and anticonvulsant drugs and premature infants with oxygen. 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subjects Animals
Anticonvulsants - pharmacology
Antiepileptic drugs
Apoptosis - drug effects
Apoptosis - physiology
Brain - cytology
Brain - drug effects
Brain - growth & development
Brain - physiology
Cell Proliferation - drug effects
Cytokines - metabolism
Development
Environment
Ethanol - toxicity
GABA-A Receptor Agonists
Humans
Hypnotics and Sedatives - pharmacology
Nerve Degeneration - chemically induced
Nerve Growth Factors - metabolism
Neurology
Neurons - drug effects
Neurons - physiology
Neuroprotective Agents - pharmacology
Oxidative Stress - drug effects
Oxidative Stress - physiology
Oxygen
Oxygen - metabolism
Oxygen - toxicity
Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors
Sedative drugs
Sodium Channel Blockers - pharmacology
title Triggers of apoptosis in the immature brain
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