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The transition into and out of adolescence is a unique developmental period during which neuronal circuits are particularly susceptible to modification by experience. Adolescence is associated with an increased incidence of anxiety disorders in humans, and an estimated 75% of adults with fear-related disorders met diagnostic criteria as children and adolescents. Conserved neural circuitry of rodents and humans has facilitated neurodevelopmental studies of behavioral and molecular processes associated with fear learning and memory that lie at the heart of many anxiety disorders. Here, we review the nonlinear developmental aspects of fear learning and memory during a transition period into and out of adolescence and provide a discussion of the molecular mechanisms that may underlie these alterations in behavior. We provide a model that may help to inform novel treatment strategies for children and adolescents with fear-related disorders., (© 2013 New York Academy of Sciences.)

The only evidence-based behavioral treatment for anxiety and stress-related disorders involves desensitization techniques that rely on principles of extinction learning. However, 40% of patients do not respond to this treatment. Efforts have focused on individual differences in treatment response, but have not examined when, during development, such treatments may be most effective. We examined fear-extinction learning across development in mice and humans. Parallel behavioral studies revealed attenuated extinction learning during adolescence. Probing neural circuitry in mice revealed altered synaptic plasticity of prefrontal cortical regions implicated in suppression of fear responses across development. The results suggest a lack of synaptic plasticity in the prefrontal regions, during adolescence, is associated with blunted regulation of fear extinction. These findings provide insight into optimizing treatment outcomes for when, during development, exposure therapies may be most effective.

A fundamental issue in psychiatric medicine is the lack of empirical evidence indicating when, during development, a treatment will be most effective for a patient. We review behavioral and brain changes that occur across development, focusing on the period of adolescence, when there is a peak in diagnosis of many psychiatric disorders. We use anxiety disorders as an example because of their high prevalence in youth (affecting as many as 1 in 10). Basic forms of fear learning, which are at the core of anxiety disorders and are the targets of behavioral therapeutics, are examined as a function of age. We also discuss how fear learning has been genetically modulated in mice and humans. Based on these findings, we provide future directions for determining the efficacy of innovative therapies and preventive strategies for anxiety disorders as a function of age and potential genetic effects inferred from mice and humans. [ABSTRACT FROM AUTHOR]