Adolescence is a period of heightened emotional reactivity and vulnerability to poor outcomes (e.g., suicide, anxiety, and depression). Recent human and animal neuroimaging studies suggest that dramatic changes in prefrontal cortical areas during adolescence are involved in these effects. The present study explored the functional implications of prefrontal cortical changes during adolescence by examining conditioned fear extinction in adolescent rats. Experiment 1 showed that preadolescent (i.e., postnatal day [P] 24), adolescent (P35), and adult (P70) rats express identical extinction acquisition following 3 white-noise conditioned stimulus (CS) and shock pairings. When tested the next day, however, adolescent rats showed almost complete failure to maintain extinction of CS-elicited freezing compared with P24 and P70 rats. It was observed in experiment 2 that following extinction, P24 and P70 rats express significantly elevated levels of phosphorylated mitogen-activated protein kinase (pMAPK) in the infralimbic cortex (IL) compared with adolescent rats. Interestingly, adolescent rats successfully exhibited long-term extinction if the amount of extinction training was doubled (experiment 3). More extinction training also led to increased phosphorylation of MAPK in the IL in these rats. These findings suggest that adolescents are less efficient in utilizing prefrontal areas, which may lead to an impairment in the maintenance of extinguished behavior.

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Studies have shown that in adult animals the medial prefrontal cortex (mPFC) is a critical brain region involved in fear regulation, with the prelimbic (PL) subregion being important for fear expression. However, few studies have examined whether the PL cortex is also involved in fear expression in infant animals. Five experiments, using immunohistochemical and temporary inactivation procedures, assessed the role of the PL in the expression of learned fear in postnatal day (PND) 18 (infant) and PND25 (juvenile) rats. We found that in juvenile rats expressing fear (measured through freezing) there was an increase in the number of phosphorylated mitogen-activated protein kinase (pMAPK)-labeled neurons in the PL; this increase was not observed in the infralimbic cortex. Furthermore, inactivation of the PL at test, using muscimol, decreased freezing in the juvenile rat. In contrast, expression of learned fear in infant rats did not require the PL, as there was neither an increase in the number of pMAPK-labeled cells in the PL nor was there any effect of PL inactivation on freezing levels. Taken together, these experiments suggest that a different neural circuitry underlies fear regulation early in life and that the lack of mPFC involvement may reflect a less flexible emotional regulation system in infant animals.

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Unlike adult memories that can be remembered for many years, memories that are formed early in life are more fragile and susceptible to being forgotten (a phenomenon known as "infantile" or "childhood" amnesia). Nonetheless, decades of research in both humans and nonhuman animals demonstrate the importance of early life experiences on later physical, mental, and emotional functioning. This raises the question of how early memories can be so influential if they cannot be recalled. This review presents one potential solution to this paradox by considering what happens to an early memory after it has been forgotten. Specifically, we describe evidence showing that these forgotten early-acquired memories have not permanently decayed from storage. Instead, there appears to be a memory "trace" that persists in the face of forgetting which continues to affect a variety of behavioral responses later in life. Excitingly, the discovery of this physical trace will allow us to explore previously untestable issues in new ways, from whether forgetting is due to a failure in retrieval or storage to how memories can be recovered after extended periods of time. A greater understanding of the characteristics of this memory trace will provide novel insights into how some memories are left behind in childhood while others are carried with us, at least in some form, for a lifetime.Memory, along with most other cognitive abilities, develops across the lifespan (Ofen and Shing 2013). While memories acquired in adulthood are generally well remembered and persistent (e.g., Gale et al. 2004), memories formed earlier in development are usually quite fragile and rapidly forgotten (a phenomenon known as "infantile" or "childhood" amnesia [Campbell and Campbell 1962;Spear and Parsons 1976;Hayne 2004;Hayne and Jack 2011]). The fact that early memories are so fragile has resulted in a great deal of controversy over the importance of early experiences on later functioning (e.g., Fraley et al. 2013). Specifically, if early experiences cannot be explicitly recalled, how can they influence an individual's functioning later in life? Although this question remains unanswered, there is an overwhelming amount of evidence supporting the idea that early experiences are critical for later functioning. For example, there is substantial evidence that the quality of maternal care experienced early in life affects the behavioral, neural, and physiological responses of the offspring as they mature. In a striking series of studies, Tottenham and colleagues examined children who experienced maternal deprivation in the first two years of life (i.e., had been reared in an orphanage). In one study it was reported that these individuals were more likely to experience depression in adolescence . Further, on a neural level, they also exhibited altered maturation of the nucleus accumbens, a structure involved in reward learning. In another study, these individuals exhibited amygdala hyperactivity as well as accelerated maturation of amygdala-prefrontal cortex connectiv...