Reward Circuitry and Motivational Deficits in Social Anxiety Disorder: What Can Be Learned From Mouse Models?

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dc.contributor.authorCarlton, Corinne N.en
dc.contributor.authorSullivan-Toole, Hollyen
dc.contributor.authorGhane, Merageen
dc.contributor.authorRichey, John A.en
dc.contributor.departmentPsychologyen
dc.date.accessioned2020-05-14T13:08:27Zen
dc.date.available2020-05-14T13:08:27Zen
dc.date.issued2020-02-26en
dc.description.abstractSocial anxiety disorder (SAD) is a common and serious psychiatric condition that typically emerges during adolescence and persists into adulthood if left untreated. Prevailing interventions focus on modulating threat and arousal systems but produce only modest rates of remission. This gap in efficacy suggests that most mainstream treatment concepts do not sufficiently target core processes involved in the onset and maintenance of SAD. This idea has further driven the development of new theoretical models that target dopamine (DA)-driven reward circuitry and motivational deficits that appear to be systematically altered in SAD. Most of the available data linking systemic alterations in DA neurobiology to SAD in humans, although abundant, remains at the level of correlational evidence. Accordingly, the purpose of this brief review is to critically evaluate the relevance of experimental work in rodent models that link details of DA function to symptoms of social anxiety. We conclude that, despite certain systematic limitations inherent in animal models, these approaches provide useful insights into human biomarkers of social anxiety including that (1) adolescence may serve as a critical period for the convergence of neurobiological and environmental factors that modify future expectations about social reward through experience dependent changes in DA-ergic circuitry, (2) females may show unique susceptibility to social anxiety symptoms when encountering relational instability that influences DA-related neural processes, and (3) separate from fear and arousal systems, the functional neurobiology of central DA systems contribute uniquely to susceptibility and maintenance of anhedonic factors relevant to human models of SAD.en
dc.format.mimetypeapplication/pdfen
dc.identifier.doihttps://doi.org/10.3389/fnins.2020.00154en
dc.identifier.eissn1662-453Xen
dc.identifier.other154en
dc.identifier.pmid32174811en
dc.identifier.urihttp://hdl.handle.net/10919/98261en
dc.identifier.volume14en
dc.language.isoenen
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectsocial anxietyen
dc.subjectanhedoniaen
dc.subjectrewarden
dc.subjectmouse modelsen
dc.subjectsocial stressen
dc.titleReward Circuitry and Motivational Deficits in Social Anxiety Disorder: What Can Be Learned From Mouse Models?en
dc.title.serialFrontiers in Neuroscienceen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten
dc.type.dcmitypeStillImageen

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Scholarly Works, Psychology
Destination Area: Adaptive Brain and Behavior (ABB)
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