Apoptotic neurodegeneration induced by ethanol in neonatal mice is associated with profound learning/memory deficits in juveniles followed by progressive functional recovery in adults
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 neurobehavioral disturbances in human Fetal Alcohol Syndrome (FAS). Here, we report binge-like exposu...
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doaj-6c70138f8bec4e86bd3a85dd522ca8d72021-03-20T04:50:11ZengElsevierNeurobiology of Disease1095-953X2004-12-01173403414Apoptotic neurodegeneration induced by ethanol in neonatal mice is associated with profound learning/memory deficits in juveniles followed by progressive functional recovery in adultsDavid F. Wozniak0Richard E. Hartman1Maureen P. Boyle2Sherri K. Vogt3Ashley R. Brooks4Tatyana Tenkova5Chainllie Young6John W. Olney7Louis J. Muglia8Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110, USADepartment of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110, USADepartment of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Obstetrics and Gynecology, Washington University School of Medicine, St. Louis, MO 63110, USADepartment of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Obstetrics and Gynecology, Washington University School of Medicine, St. Louis, MO 63110, USADepartment of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Obstetrics and Gynecology, Washington University School of Medicine, St. Louis, MO 63110, USADepartment of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110, USADepartment of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110, USADepartment of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110, USADepartment of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Obstetrics and Gynecology, Washington University School of Medicine, St. Louis, MO 63110, USA; Corresponding author. Department of Pediatrics, Washington University School of Medicine, 660 S. Euclid Avenue, PO Box 8208, St. Louis, MO 63110. Fax: +1 314 286 2893.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 neurobehavioral 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 1 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 neuroapoptotic 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.http://www.sciencedirect.com/science/article/pii/S0969996104001913ApoptosisBehaviorFetal Alcohol SyndromeHippocampusMiceThalamus |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
David F. Wozniak Richard E. Hartman Maureen P. Boyle Sherri K. Vogt Ashley R. Brooks Tatyana Tenkova Chainllie Young John W. Olney Louis J. Muglia |
spellingShingle |
David F. Wozniak Richard E. Hartman Maureen P. Boyle Sherri K. Vogt Ashley R. Brooks Tatyana Tenkova Chainllie Young John W. Olney Louis J. Muglia Apoptotic neurodegeneration induced by ethanol in neonatal mice is associated with profound learning/memory deficits in juveniles followed by progressive functional recovery in adults Neurobiology of Disease Apoptosis Behavior Fetal Alcohol Syndrome Hippocampus Mice Thalamus |
author_facet |
David F. Wozniak Richard E. Hartman Maureen P. Boyle Sherri K. Vogt Ashley R. Brooks Tatyana Tenkova Chainllie Young John W. Olney Louis J. Muglia |
author_sort |
David F. Wozniak |
title |
Apoptotic neurodegeneration induced by ethanol in neonatal mice is associated with profound learning/memory deficits in juveniles followed by progressive functional recovery in adults |
title_short |
Apoptotic neurodegeneration induced by ethanol in neonatal mice is associated with profound learning/memory deficits in juveniles followed by progressive functional recovery in adults |
title_full |
Apoptotic neurodegeneration induced by ethanol in neonatal mice is associated with profound learning/memory deficits in juveniles followed by progressive functional recovery in adults |
title_fullStr |
Apoptotic neurodegeneration induced by ethanol in neonatal mice is associated with profound learning/memory deficits in juveniles followed by progressive functional recovery in adults |
title_full_unstemmed |
Apoptotic neurodegeneration induced by ethanol in neonatal mice is associated with profound learning/memory deficits in juveniles followed by progressive functional recovery in adults |
title_sort |
apoptotic neurodegeneration induced by ethanol in neonatal mice is associated with profound learning/memory deficits in juveniles followed by progressive functional recovery in adults |
publisher |
Elsevier |
series |
Neurobiology of Disease |
issn |
1095-953X |
publishDate |
2004-12-01 |
description |
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 neurobehavioral 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 1 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 neuroapoptotic 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. |
topic |
Apoptosis Behavior Fetal Alcohol Syndrome Hippocampus Mice Thalamus |
url |
http://www.sciencedirect.com/science/article/pii/S0969996104001913 |
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