Regional Patterns of Alcohol‐Induced Neuronal Loss Depend on Genetics: Implications for Fetal Alcohol Spectrum Disorder
Background Alcohol exposure during pregnancy can kill developing neurons and lead to fetal alcohol spectrum disorder (FASD). However, affected individuals differ in their regional patterns of alcohol‐induced neuropathology. Because neuroprotective genes are expressed in spatially selective ways, the...
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Published in | Alcoholism, clinical and experimental research Vol. 42; no. 9; pp. 1627 - 1639 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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England
Wiley Subscription Services, Inc
01.09.2018
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Abstract | Background
Alcohol exposure during pregnancy can kill developing neurons and lead to fetal alcohol spectrum disorder (FASD). However, affected individuals differ in their regional patterns of alcohol‐induced neuropathology. Because neuroprotective genes are expressed in spatially selective ways, their mutation could increase the vulnerability of some brain regions, but not others, to alcohol teratogenicity. The objective of this study was to determine whether a null mutation of neuronal nitric oxide synthase (nNOS) can increase the vulnerability of some brain regions, but not others, to alcohol‐induced neuronal losses.
Methods
Immunohistochemistry identified brain regions in which nNOS is present or absent throughout postnatal development. Mice genetically deficient for nNOS (nNOS−/−) and wild‐type controls received alcohol (0.0, 2.2, or 4.4 mg/g/d) over postnatal days (PD) 4 to 9. Mice were sacrificed in adulthood (~PD 115), and surviving neurons in the olfactory bulb granular layer and brain stem facial nucleus were quantified stereologically.
Results
nNOS was expressed throughout postnatal development in olfactory bulb granule cells but was never expressed in the facial nucleus. In wild‐type mice, alcohol reduced neuronal survival to similar degrees in both cell populations. However, null mutation of nNOS more than doubled alcohol‐induced cell death in the olfactory bulb granule cells, while the mutation had no effect on the facial nucleus neurons. As a result, in nNOS−/− mice, alcohol caused substantially more cell loss in the olfactory bulb than in the facial nucleus.
Conclusions
Mutation of the nNOS gene substantially increases vulnerability to alcohol‐induced cell loss in a brain region where the gene is expressed (olfactory bulb), but not in a separate brain region, where the gene is not expressed (facial nucleus). Thus, differences in genotype may explain why some individuals are vulnerable to FASD, while others are not, and may determine the specific patterns of neuropathology in children with FASD. |
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AbstractList | BackgroundAlcohol exposure during pregnancy can kill developing neurons and lead to fetal alcohol spectrum disorder (FASD). However, affected individuals differ in their regional patterns of alcohol‐induced neuropathology. Because neuroprotective genes are expressed in spatially selective ways, their mutation could increase the vulnerability of some brain regions, but not others, to alcohol teratogenicity. The objective of this study was to determine whether a null mutation of neuronal nitric oxide synthase (nNOS) can increase the vulnerability of some brain regions, but not others, to alcohol‐induced neuronal losses.MethodsImmunohistochemistry identified brain regions in which nNOS is present or absent throughout postnatal development. Mice genetically deficient for nNOS (nNOS−/−) and wild‐type controls received alcohol (0.0, 2.2, or 4.4 mg/g/d) over postnatal days (PD) 4 to 9. Mice were sacrificed in adulthood (~PD 115), and surviving neurons in the olfactory bulb granular layer and brain stem facial nucleus were quantified stereologically.ResultsnNOS was expressed throughout postnatal development in olfactory bulb granule cells but was never expressed in the facial nucleus. In wild‐type mice, alcohol reduced neuronal survival to similar degrees in both cell populations. However, null mutation of nNOS more than doubled alcohol‐induced cell death in the olfactory bulb granule cells, while the mutation had no effect on the facial nucleus neurons. As a result, in nNOS−/− mice, alcohol caused substantially more cell loss in the olfactory bulb than in the facial nucleus.ConclusionsMutation of the nNOS gene substantially increases vulnerability to alcohol‐induced cell loss in a brain region where the gene is expressed (olfactory bulb), but not in a separate brain region, where the gene is not expressed (facial nucleus). Thus, differences in genotype may explain why some individuals are vulnerable to FASD, while others are not, and may determine the specific patterns of neuropathology in children with FASD. Background Alcohol exposure during pregnancy can kill developing neurons and lead to fetal alcohol spectrum disorder (FASD). However, affected individuals differ in their regional patterns of alcohol‐induced neuropathology. Because neuroprotective genes are expressed in spatially selective ways, their mutation could increase the vulnerability of some brain regions, but not others, to alcohol teratogenicity. The objective of this study was to determine whether a null mutation of neuronal nitric oxide synthase (nNOS) can increase the vulnerability of some brain regions, but not others, to alcohol‐induced neuronal losses. Methods Immunohistochemistry identified brain regions in which nNOS is present or absent throughout postnatal development. Mice genetically deficient for nNOS (nNOS −/− ) and wild‐type controls received alcohol (0.0, 2.2, or 4.4 mg/g/d) over postnatal days (PD) 4 to 9. Mice were sacrificed in adulthood (~PD 115), and surviving neurons in the olfactory bulb granular layer and brain stem facial nucleus were quantified stereologically. Results nNOS was expressed throughout postnatal development in olfactory bulb granule cells but was never expressed in the facial nucleus. In wild‐type mice, alcohol reduced neuronal survival to similar degrees in both cell populations. However, null mutation of nNOS more than doubled alcohol‐induced cell death in the olfactory bulb granule cells, while the mutation had no effect on the facial nucleus neurons. As a result, in nNOS −/− mice, alcohol caused substantially more cell loss in the olfactory bulb than in the facial nucleus. Conclusions Mutation of the nNOS gene substantially increases vulnerability to alcohol‐induced cell loss in a brain region where the gene is expressed (olfactory bulb), but not in a separate brain region, where the gene is not expressed (facial nucleus). Thus, differences in genotype may explain why some individuals are vulnerable to FASD, while others are not, and may determine the specific patterns of neuropathology in children with FASD. Background Alcohol exposure during pregnancy can kill developing neurons and lead to fetal alcohol spectrum disorder (FASD). However, affected individuals differ in their regional patterns of alcohol‐induced neuropathology. Because neuroprotective genes are expressed in spatially selective ways, their mutation could increase the vulnerability of some brain regions, but not others, to alcohol teratogenicity. The objective of this study was to determine whether a null mutation of neuronal nitric oxide synthase (nNOS) can increase the vulnerability of some brain regions, but not others, to alcohol‐induced neuronal losses. Methods Immunohistochemistry identified brain regions in which nNOS is present or absent throughout postnatal development. Mice genetically deficient for nNOS (nNOS−/−) and wild‐type controls received alcohol (0.0, 2.2, or 4.4 mg/g/d) over postnatal days (PD) 4 to 9. Mice were sacrificed in adulthood (~PD 115), and surviving neurons in the olfactory bulb granular layer and brain stem facial nucleus were quantified stereologically. Results nNOS was expressed throughout postnatal development in olfactory bulb granule cells but was never expressed in the facial nucleus. In wild‐type mice, alcohol reduced neuronal survival to similar degrees in both cell populations. However, null mutation of nNOS more than doubled alcohol‐induced cell death in the olfactory bulb granule cells, while the mutation had no effect on the facial nucleus neurons. As a result, in nNOS−/− mice, alcohol caused substantially more cell loss in the olfactory bulb than in the facial nucleus. Conclusions Mutation of the nNOS gene substantially increases vulnerability to alcohol‐induced cell loss in a brain region where the gene is expressed (olfactory bulb), but not in a separate brain region, where the gene is not expressed (facial nucleus). Thus, differences in genotype may explain why some individuals are vulnerable to FASD, while others are not, and may determine the specific patterns of neuropathology in children with FASD. Alcohol exposure during pregnancy can kill developing neurons and lead to fetal alcohol spectrum disorder (FASD). However, affected individuals differ in their regional patterns of alcohol-induced neuropathology. Because neuroprotective genes are expressed in spatially selective ways, their mutation could increase the vulnerability of some brain regions, but not others, to alcohol teratogenicity. The objective of this study was to determine whether a null mutation of neuronal nitric oxide synthase (nNOS) can increase the vulnerability of some brain regions, but not others, to alcohol-induced neuronal losses. Immunohistochemistry identified brain regions in which nNOS is present or absent throughout postnatal development. Mice genetically deficient for nNOS (nNOS ) and wild-type controls received alcohol (0.0, 2.2, or 4.4 mg/g/d) over postnatal days (PD) 4 to 9. Mice were sacrificed in adulthood (~PD 115), and surviving neurons in the olfactory bulb granular layer and brain stem facial nucleus were quantified stereologically. nNOS was expressed throughout postnatal development in olfactory bulb granule cells but was never expressed in the facial nucleus. In wild-type mice, alcohol reduced neuronal survival to similar degrees in both cell populations. However, null mutation of nNOS more than doubled alcohol-induced cell death in the olfactory bulb granule cells, while the mutation had no effect on the facial nucleus neurons. As a result, in nNOS mice, alcohol caused substantially more cell loss in the olfactory bulb than in the facial nucleus. Mutation of the nNOS gene substantially increases vulnerability to alcohol-induced cell loss in a brain region where the gene is expressed (olfactory bulb), but not in a separate brain region, where the gene is not expressed (facial nucleus). Thus, differences in genotype may explain why some individuals are vulnerable to FASD, while others are not, and may determine the specific patterns of neuropathology in children with FASD. |
Author | Roghair, Jasmine Todd, Dylan Bonthius, Daniel J. Sabalo, Lia Marie Karacay, Bahri Bousquet, Samantha Larimer |
AuthorAffiliation | 3 Neurology, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242 1 Neuroscience Program, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242 2 Departments of Pediatrics, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242 4 Department of Biology, Wartburg College, Waverly, Iowa 50677 |
AuthorAffiliation_xml | – name: 3 Neurology, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242 – name: 1 Neuroscience Program, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242 – name: 2 Departments of Pediatrics, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242 – name: 4 Department of Biology, Wartburg College, Waverly, Iowa 50677 |
Author_xml | – sequence: 1 givenname: Dylan surname: Todd fullname: Todd, Dylan organization: University of Iowa – sequence: 2 givenname: Daniel J. surname: Bonthius fullname: Bonthius, Daniel J. organization: Wartburg College – sequence: 3 givenname: Lia Marie surname: Sabalo fullname: Sabalo, Lia Marie organization: University of Iowa – sequence: 4 givenname: Jasmine surname: Roghair fullname: Roghair, Jasmine organization: University of Iowa – sequence: 5 givenname: Bahri surname: Karacay fullname: Karacay, Bahri organization: University of Iowa – sequence: 6 givenname: Samantha Larimer surname: Bousquet fullname: Bousquet, Samantha Larimer organization: Wartburg College – sequence: 7 givenname: Daniel J. orcidid: 0000-0001-7570-3796 surname: Bonthius fullname: Bonthius, Daniel J. email: daniel-bonthius@uiowa.edu organization: University of Iowa |
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CitedBy_id | crossref_primary_10_1016_j_alcohol_2022_02_005 crossref_primary_10_3389_fncir_2024_1408187 crossref_primary_10_3389_fpsyt_2020_580771 |
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Keywords | Neuroprotection Facial Nucleus Olfactory Bulb Neuronal Nitric Oxide Synthase Fetal Alcohol Spectrum Disorder |
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Alcohol exposure during pregnancy can kill developing neurons and lead to fetal alcohol spectrum disorder (FASD). However, affected individuals... Alcohol exposure during pregnancy can kill developing neurons and lead to fetal alcohol spectrum disorder (FASD). However, affected individuals differ in their... BackgroundAlcohol exposure during pregnancy can kill developing neurons and lead to fetal alcohol spectrum disorder (FASD). However, affected individuals... |
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SubjectTerms | Alcohol Drinking - adverse effects Alcohol Drinking - genetics Alcohol Drinking - metabolism Alcohol Drinking - pathology Alcohol use Alcohols Animals Animals, Newborn Brain Brain stem Cell death Children Ethanol - toxicity Facial Nucleus Female Fetal Alcohol Spectrum Disorder Fetal Alcohol Spectrum Disorders - genetics Fetal Alcohol Spectrum Disorders - pathology Fetal alcohol syndrome Genetics Genotypes Granular materials Granule cells Immunohistochemistry Male Mice Mice, 129 Strain Mice, Inbred C57BL Mice, Knockout Mutation Neuronal Nitric Oxide Synthase Neurons Neurons - drug effects Neurons - metabolism Neurons - pathology Neuropathology Neuroprotection Nitric oxide Nitric Oxide Synthase Type I - deficiency Nitric Oxide Synthase Type I - genetics Nitric-oxide synthase Nuclei (cytology) Olfactory Bulb Olfactory Bulb - drug effects Olfactory Bulb - metabolism Olfactory Bulb - pathology Pregnancy Random Allocation Smell Teratogenicity |
Title | Regional Patterns of Alcohol‐Induced Neuronal Loss Depend on Genetics: Implications for Fetal Alcohol Spectrum Disorder |
URI | https://onlinelibrary.wiley.com/doi/abs/10.1111%2Facer.13824 https://www.ncbi.nlm.nih.gov/pubmed/29957842 https://www.proquest.com/docview/2098579671/abstract/ https://pubmed.ncbi.nlm.nih.gov/PMC6445660 |
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