Journal
NEUROBIOLOGY OF DISEASE
Volume 17, Issue 3, Pages 403-414Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2004.08.006
Keywords
apoptosis; behavior; fetal alcohol syndrome; hippocampus; mice; thalamus
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Funding
- NIAAA NIH HHS [AA12957] Funding Source: Medline
- NICHD NIH HHS [HD37100] Funding Source: Medline
- NIDA NIH HHS [DA05072] Funding Source: Medline
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Administration of ethanol to rodents during the synaptogenesis period induces extensive apoptotic neurodegeneration in the developing brain. This neurotoxicity may explain the reduced brain mass and neuro-behavioral disturbances in human Fetal Alcohol Syndrome (FAS). Here, we report binge-like exposure of infant mice to ethanol on a single postnatal day triggered apoptotic death of neurons from diencephalic structures that comprise an extended hippocampal circuit important for spatial learning and memory. The ethanol exposure paradigm yielding these neuronal losses caused profound impairments in spatial learning and memory at I month of age. This impairment was significantly attenuated during subsequent development, indicating recovery of function. Recovery was not associated with increased neurogenesis, suggesting plastic reorganization of neuronal networks compensated for early neuronal losses. We hypothesize that neuro-apoptotic damage in homologous regions of human brain underlies cognitive deficits in FAS and the human brain of FAS victims has a similar capacity to effect functional recovery. (C) 2004 Elsevier Inc. All rights reserved.
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