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Beta-adrenergic antagonism modulates functional connectivity in the default mode network of individuals with and without autism spectrum disorder

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Abstract

The beta-adrenergic antagonist propranolol benefits some social and communication domains affected in autism spectrum disorder (ASD), and these benefits appear to be associated with increased functional connectivity (FC) in the brain during task performance. FC is implicated in ASD, with the majority of studies suggesting long distance hypo-connectivity combined with regionally specific local hyper-connectivity. The objective in the current investigation was to examine the effect of propranolol on FC at rest and determine whether ASD-specific effects exist. Participants with and without ASD attended three sessions in which propranolol, nadolol (a beta-adrenergic antagonist that does not cross the blood-brain barrier), or placebo were administered. Resting-state fMRI data were acquired, and graph theory techniques were utilized to assess additional aspects of FC. Compared to placebo, propranolol administration was associated with decreased FC in the dorsal medial prefrontal cortex subnetwork of the default mode network and increased FC in the medial temporal lobe subnetwork, regardless of diagnosis. These effects were not seen with nadolol suggesting that the alterations in FC following propranolol administration were not exclusively due to peripheral cardiovascular effects. Thus, beta-adrenergic antagonism can up- or down- regulate FC, depending on the network, and alter coordinated functional activation in the brain. These changes in information processing, as demonstrated by FC, may mediate some of the clinical and behavioral effects of beta-adrenergic antagonism previously reported in patients with ASD.

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Acknowledgments

We would like to thank all of the individuals and their families that participated in this investigation as well as the faculty and staff at the University of Missouri Brain Imaging Center, Thompson Center for Autism and Neurodevelopmental Disorders, and School of Medicine that were involved in this work. This project was supported by a grant from the Health Resources and Services Administration (1R40MC19926) and the University of Missouri, School of Medicine Mission Enhancement Fund awarded to David Q. Beversdorf.

Disclosures

John P. Hegarty II, Bradley J. Ferguson, Rachel M. Zamzow, Landon J. Rohowetz, Jeffrey D. Johnson, Shawn E. Christ, and David Q. Beversdorf declare that they have no conflict of interest. All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1975, and the applicable revisions at the time of the investigation. Informed consent was obtained from all patients for being included in the study.

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Authors and Affiliations

  1. University of Missouri, Columbia, MO, USA

    John P. Hegarty II, Bradley J. Ferguson, Rachel M. Zamzow, Landon J. Rohowetz, Jeffrey D. Johnson, Shawn E. Christ & David Q. Beversdorf

  2. Interdisciplinary Neuroscience Program, University of Missouri, Columbia, MO, USA

    John P. Hegarty II, Bradley J. Ferguson & Rachel M. Zamzow

  3. Department of Psychiatry and Behavioral Sciences, Stanford University, Palo Alto, CA, USA

    John P. Hegarty II

  4. Department of Psychological Sciences, University of Missouri, Columbia, MO, USA

    Landon J. Rohowetz, Jeffrey D. Johnson, Shawn E. Christ & David Q. Beversdorf

  5. Department of Radiology, University of Missouri School of Medicine, Columbia, MO, USA

    David Q. Beversdorf

  6. Department of Neurology, University of Missouri School of Medicine, Columbia, MO, USA

    David Q. Beversdorf

  7. Thompson Center for Autism and Neurodevelopmental Disorders, University of Missouri, Columbia, MO, USA

    David Q. Beversdorf

  8. William and Nancy Thompson Chair in Radiology, Columbia, MO, USA

    David Q. Beversdorf

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  1. John P. Hegarty II
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Hegarty, J.P., Ferguson, B.J., Zamzow, R.M. et al. Beta-adrenergic antagonism modulates functional connectivity in the default mode network of individuals with and without autism spectrum disorder. Brain Imaging and Behavior 11, 1278–1289 (2017). https://doi.org/10.1007/s11682-016-9604-8

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