Increased BDNF expression in fetal brain in the valproic acid model of autism
Human fetal exposure to valproic acid (VPA), a widely-used anti-epileptic and mood-stabilizing drug, leads to an increased incidence of behavioral and intellectual impairments including autism; VPA administration to pregnant rats and mice at gestational days 12.5 (E12.5) or E13.5 leads to autistic-l...
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| Published in | Molecular and cellular neuroscience Vol. 59; pp. 57 - 62 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.03.2014
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Human fetal exposure to valproic acid (VPA), a widely-used anti-epileptic and mood-stabilizing drug, leads to an increased incidence of behavioral and intellectual impairments including autism; VPA administration to pregnant rats and mice at gestational days 12.5 (E12.5) or E13.5 leads to autistic-like symptoms in the offspring and is widely used as an animal model for autism. We report here that this VPA administration protocol transiently increased both BDNF mRNA and BDNF protein levels 5–6-fold in the fetal mouse brain. VPA exposure in utero induced smaller increases in the expression of mRNA encoding the other neurotrophins, NT3 (2.5-fold) and NT4 (2-fold). Expression of the neurotrophin receptors, trkA, trkB and trkC were minimally affected, while levels of the low-affinity neurotrophin receptor, p75NTR, doubled. Of the nine 5′-untranslated exons of the mouse BDNF gene, only expression of exons I, IV and VI was stimulated by VPA in utero. In light of the well-established role of BDNF in regulating neurogenesis and the laminar fate of postmitotic neurons in the developing cortex, an aberrant increase in BDNF expression in the fetal brain may contribute to VPA-induced cognitive disorders by altering brain development. |
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| AbstractList | Human fetal exposure to valproic acid (VPA), a widely-used anti-epileptic
and mood-stabilizing drug, leads to an increased incidence of behavioral and
intellectual impairments including autism; VPA administration to pregnant rats
and mice at gestational days 12.5 (E12.5) or E13.5 leads to autistic-like
symptoms in the offspring and is widely used as an animal model for autism. We
report here that this VPA administration protocol transiently increased both
BDNF mRNA and BDNF protein levels 5–6-fold in the fetal mouse brain. VPA
exposure
in utero
induced smaller increases in the expression
of mRNA encoding the other neurotrophins, NT3 (2.5-fold) and NT4 (2-fold).
Expression of the neurotrophin receptors, trkA, trkB and trkC were minimally
affected, while levels of the low-affinity neurotrophin receptor,
p75
NTR
, doubled. Of the nine 5′-untranslated exons of the
mouse BDNF gene, only expression of exons I, IV and VI was stimulated by VPA
in utero
. In light of the well-established role of BDNF in
regulating neurogenesis and the laminar fate of postmitotic neurons in the
developing cortex, an aberrant increase in BDNF expression in the fetal brain
may contribute to VPA-induced cognitive disorders by altering brain
development. Human fetal exposure to valproic acid (VPA), a widely-used anti-epileptic and mood-stabilizing drug, leads to an increased incidence of behavioral and intellectual impairments including autism; VPA administration to pregnant rats and mice at gestational days 12.5 (E12.5) or E13.5 leads to autistic-like symptoms in the offspring and is widely used as an animal model for autism. We report here that this VPA administration protocol transiently increased both BDNF mRNA and BDNF protein levels 5-6-fold in the fetal mouse brain. VPA exposure in utero induced smaller increases in the expression of mRNA encoding the other neurotrophins, NT3 (2.5-fold) and NT4 (2-fold). Expression of the neurotrophin receptors, trkA, trkB and trkC were minimally affected, while levels of the low-affinity neurotrophin receptor, p75(NTR), doubled. Of the nine 5'-untranslated exons of the mouse BDNF gene, only expression of exons I, IV and VI was stimulated by VPA in utero. In light of the well-established role of BDNF in regulating neurogenesis and the laminar fate of postmitotic neurons in the developing cortex, an aberrant increase in BDNF expression in the fetal brain may contribute to VPA-induced cognitive disorders by altering brain development. Human fetal exposure to valproic acid (VPA), a widely-used anti-epileptic and mood-stabilizing drug, leads to an increased incidence of behavioral and intellectual impairments including autism; VPA administration to pregnant rats and mice at gestational days 12.5 (E12.5) or E13.5 leads to autistic-like symptoms in the offspring and is widely used as an animal model for autism. We report here that this VPA administration protocol transiently increased both BDNF mRNA and BDNF protein levels 5-6-fold in the fetal mouse brain. VPA exposure in utero induced smaller increases in the expression of mRNA encoding the other neurotrophins, NT3 (2.5-fold) and NT4 (2-fold). Expression of the neurotrophin receptors, trkA, trkB and trkC were minimally affected, while levels of the low-affinity neurotrophin receptor, p75NTR, doubled. Of the nine 5'-untranslated exons of the mouse BDNF gene, only expression of exons I, IV and VI was stimulated by VPA in utero. In light of the well-established role of BDNF in regulating neurogenesis and the laminar fate of postmitotic neurons in the developing cortex, an aberrant increase in BDNF expression in the fetal brain may contribute to VPA-induced cognitive disorders by altering brain development. |
| Author | Roby, Clinton D. Krueger, Bruce K. Almeida, Luis E.F. |
| AuthorAffiliation | c Program in Neuroscience, University of Maryland Baltimore, Baltimore, Maryland 21201 a Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201 b Department of Psychiatry, University of Maryland School of Medicine, Baltimore, Maryland 21201 |
| AuthorAffiliation_xml | – name: a Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201 – name: b Department of Psychiatry, University of Maryland School of Medicine, Baltimore, Maryland 21201 – name: c Program in Neuroscience, University of Maryland Baltimore, Baltimore, Maryland 21201 |
| Author_xml | – sequence: 1 givenname: Luis E.F. surname: Almeida fullname: Almeida, Luis E.F. organization: Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA – sequence: 2 givenname: Clinton D. surname: Roby fullname: Roby, Clinton D. organization: Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA – sequence: 3 givenname: Bruce K. surname: Krueger fullname: Krueger, Bruce K. email: bkrueger@umaryland.edu organization: Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24480134$$D View this record in MEDLINE/PubMed |
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| Keywords | Neurotrophin trkB Brain-derived neurotrophic factor BDNF VPA Brain development Gene promoters NGF NT3 Autism spectrum disorder ELISA NT4 |
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| Snippet | Human fetal exposure to valproic acid (VPA), a widely-used anti-epileptic and mood-stabilizing drug, leads to an increased incidence of behavioral and... Human fetal exposure to valproic acid (VPA), a widely-used anti-epileptic and mood-stabilizing drug, leads to an increased incidence of behavioral and... |
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| SubjectTerms | Animals Autism spectrum disorder Autistic Disorder - chemically induced Autistic Disorder - metabolism Brain - drug effects Brain - embryology Brain - metabolism Brain development Brain-derived neurotrophic factor Brain-Derived Neurotrophic Factor - genetics Brain-Derived Neurotrophic Factor - metabolism Female Fetus - drug effects Fetus - metabolism Gene promoters Maternal-Fetal Exchange Mice Mice, Inbred C57BL Neurotrophin Pregnancy Receptors, Nerve Growth Factor - genetics Receptors, Nerve Growth Factor - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Valproic Acid - pharmacology Valproic Acid - toxicity VPA |
| Title | Increased BDNF expression in fetal brain in the valproic acid model of autism |
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