Does Anhedonia Presage Increased Risk of Posttraumatic Stress Disorder?

Authors

Victoria B. Risbrough, University of California, San Diego
Laura Glynn, Chapman UniversityFollow
Elysia P. Davis, University of California, Irvine
Curt A. Sandman, University of California, Irvine
Andre Obenaus, University of California, Irvine
Hal S. Stern, University of California, Irvine
David B. Keator, University of California, Irvine
Michael A. Yassa, University of California, Irvine
Tallie Z. Baram, University of California, Irvine
Dewleen G. Baker, University of California, San Diego

Files

Description

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.

ISBN

978-3-319-94824-9

Publication Date

2018

Publisher

Springer

City

Cham, Switzerland

Disciplines

Animals | Biological Psychology | Cognitive Psychology | Developmental Psychology | Mental Disorders | Nervous System | Other Mental and Social Health | Other Psychiatry and Psychology | Other Psychology | Psychiatric and Mental Health | Psychological Phenomena and Processes

Comments

In Eric Vermetten, Dewleen G. Baker, and Victoria B. Risbrough (Eds.), Behavioral Neurobiology of PTSD. Current Topics in Behavioral Neurosciences (volume 38). Dr. Glynn's chapter begins on page 249.

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Recommended Citation

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

Copyright

Springer