Fetal Alcohol Spectrum Disorder: Potential Role of Endocannabinoids Signaling
One of the unique features of prenatal alcohol exposure in humans is impaired cognitive and behavioral function resulting from damage to the central nervous system (CNS), which leads to a spectrum of impairments referred to as fetal alcohol spectrum disorder (FASD). Human FASD phenotypes can be repr...
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| Format: | Article |
| Language: | English |
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MDPI AG
2015-10-01
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| Series: | Brain Sciences |
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| Online Access: | http://www.mdpi.com/2076-3425/5/4/456 |
| _version_ | 1818520645257920512 |
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| author | Balapal S. Basavarajappa |
| author_facet | Balapal S. Basavarajappa |
| author_sort | Balapal S. Basavarajappa |
| collection | DOAJ |
| description | One of the unique features of prenatal alcohol exposure in humans is impaired cognitive and behavioral function resulting from damage to the central nervous system (CNS), which leads to a spectrum of impairments referred to as fetal alcohol spectrum disorder (FASD). Human FASD phenotypes can be reproduced in the rodent CNS following prenatal ethanol exposure. Several mechanisms are expected to contribute to the detrimental effects of prenatal alcohol exposure on the developing fetus, particularly in the developing CNS. These mechanisms may act simultaneously or consecutively and differ among a variety of cell types at specific developmental stages in particular brain regions. Studies have identified numerous potential mechanisms through which alcohol can act on the fetus. Among these mechanisms are increased oxidative stress, mitochondrial damage, interference with the activity of growth factors, glia cells, cell adhesion molecules, gene expression during CNS development and impaired function of signaling molecules involved in neuronal communication and circuit formation. These alcohol-induced deficits result in long-lasting abnormalities in neuronal plasticity and learning and memory and can explain many of the neurobehavioral abnormalities found in FASD. In this review, the author discusses the mechanisms that are associated with FASD and provides a current status on the endocannabinoid system in the development of FASD. |
| first_indexed | 2024-12-11T01:40:13Z |
| format | Article |
| id | doaj.art-1d40239c90674db1a5a5dfb9fd887e13 |
| institution | Directory Open Access Journal |
| issn | 2076-3425 |
| language | English |
| last_indexed | 2024-12-11T01:40:13Z |
| publishDate | 2015-10-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Brain Sciences |
| spelling | doaj.art-1d40239c90674db1a5a5dfb9fd887e132022-12-22T01:25:04ZengMDPI AGBrain Sciences2076-34252015-10-015445649310.3390/brainsci5040456brainsci5040456Fetal Alcohol Spectrum Disorder: Potential Role of Endocannabinoids SignalingBalapal S. Basavarajappa0Division of Analytical Psychopharmacology, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USAOne of the unique features of prenatal alcohol exposure in humans is impaired cognitive and behavioral function resulting from damage to the central nervous system (CNS), which leads to a spectrum of impairments referred to as fetal alcohol spectrum disorder (FASD). Human FASD phenotypes can be reproduced in the rodent CNS following prenatal ethanol exposure. Several mechanisms are expected to contribute to the detrimental effects of prenatal alcohol exposure on the developing fetus, particularly in the developing CNS. These mechanisms may act simultaneously or consecutively and differ among a variety of cell types at specific developmental stages in particular brain regions. Studies have identified numerous potential mechanisms through which alcohol can act on the fetus. Among these mechanisms are increased oxidative stress, mitochondrial damage, interference with the activity of growth factors, glia cells, cell adhesion molecules, gene expression during CNS development and impaired function of signaling molecules involved in neuronal communication and circuit formation. These alcohol-induced deficits result in long-lasting abnormalities in neuronal plasticity and learning and memory and can explain many of the neurobehavioral abnormalities found in FASD. In this review, the author discusses the mechanisms that are associated with FASD and provides a current status on the endocannabinoid system in the development of FASD.http://www.mdpi.com/2076-3425/5/4/456fetal alcohollearning and memoryCB1 receptorsbrain developmentsynaptic plasticityintellectual disability |
| spellingShingle | Balapal S. Basavarajappa Fetal Alcohol Spectrum Disorder: Potential Role of Endocannabinoids Signaling Brain Sciences fetal alcohol learning and memory CB1 receptors brain development synaptic plasticity intellectual disability |
| title | Fetal Alcohol Spectrum Disorder: Potential Role of Endocannabinoids Signaling |
| title_full | Fetal Alcohol Spectrum Disorder: Potential Role of Endocannabinoids Signaling |
| title_fullStr | Fetal Alcohol Spectrum Disorder: Potential Role of Endocannabinoids Signaling |
| title_full_unstemmed | Fetal Alcohol Spectrum Disorder: Potential Role of Endocannabinoids Signaling |
| title_short | Fetal Alcohol Spectrum Disorder: Potential Role of Endocannabinoids Signaling |
| title_sort | fetal alcohol spectrum disorder potential role of endocannabinoids signaling |
| topic | fetal alcohol learning and memory CB1 receptors brain development synaptic plasticity intellectual disability |
| url | http://www.mdpi.com/2076-3425/5/4/456 |
| work_keys_str_mv | AT balapalsbasavarajappa fetalalcoholspectrumdisorderpotentialroleofendocannabinoidssignaling |