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Behavioral Neurobiology of PTSD pp 249–265Cite as

Does Anhedonia Presage Increased Risk of Posttraumatic Stress Disorder?

Adolescent Anhedonia and Posttraumatic Disorders

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Part of the book series: Current Topics in Behavioral Neurosciences ((CTBN,volume 38))

Abstract

Anhedonia, the reduced ability to experience pleasure, is a dimensional entity linked to multiple neuropsychiatric disorders, where it is associated with diminished treatment response, reduced global function, and increased suicidality. It has been suggested that anhedonia and the related disruption in reward processing may be critical precursors to development of psychiatric symptoms later in life. Here, we examine cross-species evidence supporting the hypothesis that early life experiences modulate development of reward processing, which if disrupted, result in anhedonia. Importantly, we find that anhedonia may confer risk for later neuropsychiatric disorders, especially posttraumatic stress disorder (PTSD). Whereas childhood trauma has long been associated with increased anhedonia and increased subsequent risk for trauma-related disorders in adulthood, here we focus on an additional novel, emerging direct contributor to anhedonia in rodents and humans: fragmented, chaotic environmental signals (“FRAG”) during critical periods of development. In rodents, recent data suggest that adolescent anhedonia may derive from aberrant pleasure/reward circuit maturation. In humans, recent longitudinal studies support that FRAG is associated with increased anhedonia in adolescence. Both human and rodent FRAG exposure also leads to aberrant hippocampal function. Prospective studies are underway to examine if anhedonia is also a marker of PTSD risk. These preliminary cross-species studies provide a critical construct for future examination of the etiology of trauma-related symptoms in adults and for and development of prophylactic and therapeutic interventions. In addition, longitudinal studies of reward circuit development with and without FRAG will be critical to test the mechanistic hypothesis that early life FRAG modifies reward circuitry with subsequent consequences for adolescent-emergent anhedonia and contributes to risk and resilience to trauma and stress in adulthood.

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Acknowledgements

Support for this work includes NIMH P50MH096889 (Drs. Baram, Glynn, Davis, Sandman, Stern, Keator, and Baram) and MH73136 (Baram), a VA Merit Award and NIH R01AA026560 (Risbrough), project No. SDR 09-0128 (Drs. Baker and Risbrough) from the Veterans Administration Health Service Research and Development, the US Marine Corps and Navy Bureau of Medicine and Surgery (Drs. Baker, and Risbrough).

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Authors and Affiliations

  1. Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA

    Victoria B. Risbrough & Dewleen G. Baker

  2. Center of Excellence for Stress and Mental Health, San Diego Veterans Administration, La Jolla, CA, USA

    Victoria B. Risbrough & Dewleen G. Baker

  3. Department of Psychology, Chapman University, Orange, CA, USA

    Laura M. Glynn

  4. Department of Psychiatry and Human Behavior, University of California, Irvine, CA, USA

    Laura M. Glynn, Elysia P. Davis, Curt A. Sandman & David B. Keator

  5. Department of Psychology, University of Denver, Denver, CO, USA

    Elysia P. Davis

  6. Department of Pediatrics, University of California, Irvine, CA, USA

    Andre Obenaus & Tallie Z. Baram

  7. Department of Statistics, University of California, Irvine, CA, USA

    Hal S. Stern

  8. Department of Computer Science, University of California, Irvine, CA, USA

    David B. Keator

  9. Department of Neurology, University of California, Irvine, CA, USA

    David B. Keator & Tallie Z. Baram

  10. Department of Neurobiology and Behavior, University of California, Irvine, CA, USA

    Michael A. Yassa

  11. Center for the Neurobiology of Learning and Memory, University of California, Irvine, CA, USA

    Michael A. Yassa

  12. Department of Anatomy/Neurobiology, University of California, Irvine, CA, USA

    Tallie Z. Baram

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  1. Victoria B. Risbrough
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  2. Laura M. Glynn
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  4. Curt A. Sandman
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  5. Andre Obenaus
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  6. Hal S. Stern
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  7. David B. Keator
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  8. Michael A. Yassa
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  9. Tallie Z. Baram
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  10. Dewleen G. Baker
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Corresponding author

Correspondence to Victoria B. Risbrough .

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Editors and Affiliations

  1. Department Psychiatry, Leiden University Medical Center, Leiden, The Netherlands

    Eric Vermetten

  2. Department of Psychiatry, UC San Diego School of Medicine, San Diego, CA, USA

    Dewleen G. Baker

  3. Department of Psychiatry, University of California San Diego, La Jolla, CA, USA

    Victoria B. Risbrough

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Risbrough, V.B. et al. (2018). Does Anhedonia Presage Increased Risk of Posttraumatic Stress Disorder?. In: Vermetten, E., Baker, D.G., Risbrough, V.B. (eds) Behavioral Neurobiology of PTSD. Current Topics in Behavioral Neurosciences, vol 38. Springer, Cham. https://doi.org/10.1007/7854_2018_51

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