Prenatal exposure to valproic acid leads to reduced expression of synaptic adhesion molecule neuroligin 3 in mice
Abstract
In rodents, a single administration of valproic acid (VPA) in utero leads to developmental delays and lifelong deficits in motor performance, social behavior, and anxiety-like behavior in the offspring. Recently, we have demonstrated that VPA mice show alterations in postnatal growth and development, and deficits in olfactory discrimination and social behavior early in development. Based on behavioral and molecular parallels between VPA rodents and individuals with autism, maternal challenge with VPA has been suggested to be a good animal model of autism. Neuroligins (NLGN) are a family of postsynaptic cell-adhesion molecules that play a role in synaptic maturation through association with their presynaptic partners, the neurexins (NRXN). Both NLGNs and NRXN members have been implicated in genetic studies of autism. In the present study, we examined changes at the level of expression of NLGN and NRXN mRNAs in the adult brain from mice exposed in utero to VPA. Mouse brain tissue was processed using in situ hybridization and analyzed with densitometry to examine expression of three NLGN genes (NLGN1, NLGN2, and NLGN3) and three NRXN genes (NRXN1, NRXN2, and NRXN3). Expression levels of NLGN1, NLGN2, NRXN1, NRXN2, and NRXN3 were observed to be similar in VPA and control mice. NLGN3 mRNA expression was found to be significantly lower in the VPA mice relative to control animals in hippocampal subregions, cornu ammonis (CA1) and dentate gyrus, and somatosensory cortex. This lowered expression may be linked to autistic-like behavioral phenotype observed in the VPA mice.
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Mice prenatally exposed to valproate show downregulation of NLGN3 in hippocampal subregions and the somatosensory cortex.
“a downregulation of NLGN3 was observed in hippocampal subregions and the somatosensory cortex of mice prenatally exposed to valproate.91”
From Autism risk factors: genes, environment, and gene-environment interactions (2012) · cites this paper as [91]
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Retracted
- Authors
- Kolozsi, E., Mackenzie, R. N., Roullet, F. I., Decatanzaro, D., & Foster, J. A.
- Affiliations
- St. Joseph’s Healthcare Hamilton (CA)
- McMaster University (CA)
- Corresponding author
- Foster, J.A.
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2009-11
- Volume
- 163
- Issue
- 4
- Pages
- 1201-1210
- ISSN
- 0306-4522 (ISSN-L)
- OpenAlex
- W2051426370
- Cited by
- 110
- References
- 65
- Citations by year
- 2026: 1 · 2024: 2 · 2023: 2 · 2022: 10 · 2021: 7 · 2020: 8 · 2019: 5 · 2018: 8 · 2017: 4 · 2016: 10 · 2015: 11 · 2014: 4 · 2013: 12 · 2012: 9
- FWCI
- 4.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- valproic acid, prenatal drug exposure, neuroligin-3, neuroligins, neurexin, autism model, synaptic adhesion molecules, hippocampus, somatosensory cortex, gene expression, autism-like behavior
- MeSH terms
- Animals, Autoradiography, Brain, Calcium-Binding Proteins, Female, Membrane Proteins, Nerve Tissue Proteins, Pregnancy, Prenatal Exposure Delayed Effects, RNA, Messenger, Valproic Acid, Cell Adhesion Molecules, Neuronal, In Situ Hybridization, GABA Agents, Neural Cell Adhesion Molecules, Mice
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