Cited by 63Autism Spectrum Disorder ResearchGenetics and Neurodevelopmental DisordersNeuroendocrine regulation and behavior

Mapk/Erk activation in an animal model of social deficits shows a possible link to autism

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Faridar, Alireza, Jones-Davis, Dorothy, Rider, Eric, Li, Jiang, Gobius, Ilan, Morcom, Laura, Richards, Linda J, Sen, Saunak +1 more·2014·Molecular Autism

Abstract

BACKGROUND: There is converging preclinical and clinical evidence to suggest that the extracellular signal-regulated kinase (ERK) signaling pathway may be dysregulated in autism spectrum disorders. METHOD: We evaluated Mapk/Erk1/2, cellular proliferation and apoptosis in BTBR mice, as a preclinical model of Autism. We had previously generated 410 F2 mice from the cross of BTBR with B6. At that time, six different social behaviors in all F2 mice were evaluated and scored. In this study, eight mice at each extreme of the social behavioral spectrum were selected and the expression and activity levels of Mapk/Erk in the prefrontal cortex and cerebellum of these mice were compared. Finally, we compared the Mapk/Erk signaling pathway in brain and lymphocytes of the same mice, testing for correlation in the degree of kinase activation across these separate tissues. RESULTS: Levels of phosphorylated Erk (p-Erk) were significantly increased in the brains of BTBR versus control mice. We also observed a significant association between juvenile social behavior and phosphorylated mitogen-activated protein kinase kinase (p-Mek) and p-Erk levels in the prefrontal cortex but not in the cerebellum. In contrast, we did not find a significant association between social behavior and total protein levels of either Mek or Erk. We also tested whether steady-state levels of Erk activation in the cerebral cortex in individual animals correlated with levels of Erk activation in lymphocytes, finding a significant relationship for this signaling pathway. CONCLUSION: These observations suggest that dysregulation of the ERK signaling pathway may be an important mediator of social behavior, and that measuring activation of this pathway in peripheral lymphocytes may serve as a surrogate marker for central nervous system (CNS) ERK activity, and possibly autistic behavior.

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  • Dysregulation of MAPK signaling has been reported in transgenic mice carrying the 16p11.2 microdeletion and in other mouse models of social impairment.

    “The dysregulation of MAPK signaling has also been reported in transgenic mice carrying the ASD-associated microdeletion of 16p11.2 (Blizinsky et al., 2016; Pucilowska et al., 2015) and in other mouse models of social impairment (Faridar et al., 2014).”

    From Getting to the cores of autism (2019) · cites this paper as Faridar et al., 2014

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Authors
Faridar, A., Jones-Davis, D., Rider, E., Li, J., Gobius, I., Morcom, L., Richards, L. J., Sen, S., & Sherr, E. H.
Affiliations
  • University of California, San Francisco (US)
  • The University of Queensland (AU)
Corresponding author
Sherr, Elliott H
Venue
Molecular Autism
Published
2014-12
Volume
5
Issue
1
Pages
57-57
ISSN
2040-2392 (ISSN-L)
OpenAlex
W2111840774
Cited by
63
References
33
Citations by year
2026: 5 · 2025: 3 · 2024: 6 · 2023: 3 · 2022: 6 · 2021: 6 · 2020: 6 · 2019: 5 · 2018: 9 · 2017: 9 · 2016: 4 · 2015: 1
FWCI
2.60
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Molecular Autism (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
  • Pfizer
  • Medical Research Council
  • National Health and Medical Research Council (1048849)
  • National Institute of Neurological Disorders and Stroke (R01NS058721)
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
  • Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
Keywords
ERK signaling, ERK1/2 MAPK, autism spectrum disorder, social behavior deficits, BTBR mice, prefrontal cortex, cerebellum, MEK phosphorylation, lymphocytes, kinase activation, surrogate markers, cell proliferation, apoptosis

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