Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2013 Mar-Apr:36:17-35.
doi: 10.1016/j.ntt.2012.08.007. Epub 2012 Sep 7.

Using mouse models of autism spectrum disorders to study the neurotoxicology of gene-environment interactions

Jared J Schwartzer  1 , Claire M Koenig, Robert F Berman
Affiliations
Review

Using mouse models of autism spectrum disorders to study the neurotoxicology of gene-environment interactions

Jared J Schwartzer et al. Neurotoxicol Teratol. 2013 Mar-Apr.

Abstract

To better study the role of genetics in autism, mouse models have been developed which mimic the genetics of specific autism spectrum and related disorders. These models have facilitated research on the role genetic susceptibility factors in the pathogenesis of autism in the absence of environmental factors. Inbred mouse strains have been similarly studied to assess the role of environmental agents on neurodevelopment, typically without the complications of genetic heterogeneity of the human population. What has not been as actively pursued, however, is the methodical study of the interaction between these factors (e.g., gene and environmental interactions in neurodevelopment). This review suggests that a genetic predisposition paired with exposure to environmental toxicants plays an important role in the etiology of neurodevelopmental disorders including autism, and may contribute to the largely unexplained rise in the number of children diagnosed with autism worldwide. Specifically, descriptions of the major mouse models of autism and toxic mechanisms of prevalent environmental chemicals are provided followed by a discussion of current and future research strategies to evaluate the role of gene and environment interactions in neurodevelopmental disorders.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Current knowledge of neurotoxic chemicals. Of the 80,000 plus registered chemicals known to exist in the environment, only a fraction have been evaluated for neurotoxicity, and even fewer for neurodevelopmental toxicity in humans. Although the diagram does not represent the true neurodevelopmental potential of these chemicals, it does indicate the magnitude of the environmental threat to human health and the need for continued research.
Figure 2
Figure 2
Complexity of gene and environment interactions in developmental disorders. Several environmental toxins have the potential to modify gene expression via epigenetic mechanisms (e.g., DNA methylation), or by directly interfering with many critical systems for normal brain development, including the endocrine system, central nervous system, and immune system. Disruption along these pathways can result in complex behavioral outcomes, and may contribute to the etiology of neurodevelopmental disorders including autism.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Abrahams BS, Geschwind DH. Advances in autism genetics: on the threshold of a new neurobiology. Nature reviews. Genetics. 2008;9(5):341–355. - PMC - PubMed
    1. Adams J, Vorhees CV, et al. Developmental neurotoxicity of anticonvulsants: human and animal evidence on phenytoin. Neurotoxicol Teratol. 1990;12(3):203–214. - PubMed
    1. Ahlbom J, Fredriksson A, et al. Neonatal exposure to a type-I pyrethroid (bioallethrin) induces dose-response changes in brain muscarinic receptors and behaviour in neonatal and adult mice. Brain Res. 1994;645(1–2):318–324. - PubMed
    1. Alkondon M, Costa AC, et al. Selective blockade of NMDA-activated channel currents may be implicated in learning deficits caused by lead. FEBS Lett. 1990;261(1):124–130. - PubMed
    1. Allen JR, Barsotti DA. The effects of transplacental and mammary movement of PCBs on infant rhesus monkeys. Toxicology. 1976;6(3):331–340. - PubMed

LinkOut - more resources