Search

Episodic memory is critical to human functioning. In adults, episodic memory involves a distributed neural circuit in which the hippocampus plays a central role. As episodic memory abilities continue to develop across childhood and into adolescence, studying episodic memory maturation can provide insight into the development and construction of these hippocampal networks, and ultimately clues to their function in adulthood. While past developmental studies have shown that the hippocampus helps to support memory in middle childhood and adolescence, the extent to which ongoing maturation within the hippocampus contributes to developmental change in episodic memory abilities remains unclear. In contrast, slower maturing regions, such as the PFC, have been suggested to be the neurobiological locus of memory improvements into adolescence. However, it is also possible that the methods used to detect hippocampal development during middle childhood and adolescence are not sensitive enough. Here, we examine how temporal covariance (or differentiation) in voxel representations within anterior and posterior hippocampus change with age to support the development of detailed recollection in male and female developing humans. We find age-related increases in the distinctiveness of temporal activation profiles in the posterior, but not anterior, hippocampus. Second, we show that this measure of granularity, when present during postencoding rest periods, correlates with the recall of detailed memories of preceding stimuli several weeks postencoding, suggesting that granularity may promote memory stabilization.SIGNIFICANCE STATEMENT Studying hippocampal maturation can provide insight into episodic memory development, as well as clues to episodic functioning in adulthood. Past work has shown evidence both for and against hippocampal contributions to age-related improvements in memory performance, but has relied heavily on univariate approaches (averaging activity across hippocampal voxels), which may not be sensitive to nuanced developmental change. Here we use a novel approach, examining time signatures in individual hippocampal voxels to reveal regionally specific (anterior vs posterior hippocampus) differences in the distinctiveness (granularity) of temporal activation profiles across development. Importantly, posterior hippocampus granularity during windows of putative memory stabilization was associated with long-term memory specificity. This suggests that the posterior hippocampus gradually builds the capacity to support detailed episodic recall.

Parental input shapes youth self‐regulation development, and a lack of sensitive caregiving is a risk factor for youth mental health problems. Parents may shape youth regulation through their influence over biological (including neural) and behavioral development during childhood at both micro (moment‐to‐moment) and macro (global) levels. Prior studies have shown that micro‐level parent‐child interactions shape youth's biology contributing to youth mental health. However, it remains unclear whether prior disrupted/absent care affects those moment‐to‐moment parent‐youth interactions in ways that increase risk for youth psychopathology. In the current study, we calculated transfer entropy on cardiac data from parent‐youth dyads where the youth had either been exposed to disrupted care prior to adoption or not. Transfer Entropy (TE) tracks information flow between two signals, enhancing quantification of directional coupling, allowing for the examination of parent‐child and child‐parent influences. Using this novel approach, we identified lower cardiac information transfer from youth‐to‐parents in dyads where the youth had been exposed to disrupted/absent early care. Moreover we showed that the degree to which the parent's physiology changed in response to youth's physiology was negatively related to the youth's mental health, representing a potential pathway for elevated mental health risk in populations exposed to disrupted/absent early care. [ABSTRACT FROM AUTHOR]

Gastrointestinal and mental disorders are highly comorbid, and animal models have shown that both can be caused by early adversity (e.g., parental deprivation). Interactions between the brain and bacteria that live within the gastrointestinal system (the microbiome) underlie adversity–gastrointestinal–anxiety interactions, but these links have not been investigated during human development. In this study, we utilized data from a population of 344 youth (3–18 years old) who were raised with their biological parents or were exposed to early adverse caregiving experiences (i.e., institutional or foster care followed by international adoption) to explore adversity–gastrointestinal–anxiety associations. In Study 1, we demonstrated that previous adverse care experiences were associated with increased incidence of gastrointestinal symptoms in youth. Gastrointestinal symptoms were also associated with concurrent and future anxiety (measured across 5 years), and those gastrointestinal symptoms mediated the adversity–anxiety association at Time 1. In a subsample of children who provided both stool samples and functional magnetic resonance imaging of the brain (Study 2, which was a "proof-of-principle"), adversity was associated with changes in diversity (both alpha and beta) of microbial communities, and bacteria levels (adversity-associated and adversity-independent) were correlated with prefrontal cortex activation to emotional faces. Implications of these data for supporting youth mental health are discussed. [ABSTRACT FROM AUTHOR]

Early adversity increases the risk of nearly all mental health disorders. Although tractable animal models exist to probe the psychobiology of early adversity, the empirical research has focused largely on adult outcomes. In the current studies we examined how early exposure to the stress hormone corticosterone (CORT) affects the maturation of fear extinction in infant rats. Whereas juvenile and adult rodents exhibit extinction learning that is relapse-prone (i.e., they show renewal and reinstatement of extinguished fear), under typical rearing conditions the extinction system in infant rats appears to be relapse-resistant (i.e., extinction leads to a permanent reduction in conditioned fear). In the current studies we tested the hypothesis that chronically exposing infant rats to CORT, either indirectly (through maternal drinking water) or directly (via insertion of an osmotic pump), leads to an early transition into the adult-like extinction system (i.e., evidence of the renewal effect). Although some differences were observed between the 2 methods of CORT exposure, the data showed that infants exposed to CORT via either method exhibited premature emergence of adult-like extinction learning (i.e., they exhibited the renewal effect). The theoretical implications of these findings for typical and abnormal development of emotion learning systems, as well as their practical applications in the context of prevention and treatment of mental health disorders, are discussed. [ABSTRACT FROM AUTHOR]

Recent studies have shown that chronic early life stress results in precocious expression of the adult-like phenotype of fear retention and inhibition. However, it is unknown whether the experience of acute early trauma has the same effects as exposure to chronic early stress. In the present study, a 24-hr period of maternal deprivation on postnatal day (P) 9 was used as an acute early life stressor. In infancy (P16-17), maternally deprived and standard-reared rats were conditioned to fear a noise paired with shock. In Experiments 1 and 2, fear to the noise was then extinguished before rats were tested for context-mediated fear renewal or stress-induced fear reinstatement. In Experiments 3a and 3b, conditioned rats were tested for fear retention 1, 7, or 14 days after training. Whereas standard-reared infants exhibited relapse-resistant extinction and infantile amnesia (i.e., behaviors typical of their age), maternally deprived infants exhibited the renewal and reinstatement effects (i.e., relapse-prone extinction) and showed good retention of fear over the 7- and 14-day intervals (i.e., infantile amnesia was reduced). In other words, similar to rats exposed to chronic early life stress, rats exposed to acute early stress expressed an adult-like profile of fear retention and inhibition during infancy. These findings suggest that similar mechanisms might be involved in the effects of acute and chronic stress on emotional development, and may have implications for our understanding and treatment of emotional disorders associated with early adversity. [ABSTRACT FROM AUTHOR]

Recent studies in rats have shown that extinction occurring early in life is resistant to relapse and may represent the erasure of fear memories. In the present study we examined the effects of early life stress on extinction in the developing rat, which could have important implications for the treatment of anxiety disorders in those who have experienced early life stress. In the present study, we used maternal- separation on postnatal days (P) 2-14 as an early life stressor. On P17, maternally separated and standard-reared animals were trained to fear a noise associated with a footshock. The fear of this noise was then extinguished (through repeated nonreinforced noise presentations) on P18. Animals were tested for contextually mediated, stress-mediated, and GABA-mediated fear relapse the day after extinction. We found that young animals exposed to maternal-separation were more likely to exhibit context- and stress-mediated relapse after extinction than standard-reared animals (Experiments 1 and 2). Further, unlike standard-reared animals, maternally separated rats exhibited a return of fear when the inhibitory neurotransmitter GABA was blocked at test (Experiment 3). These effects were not the result of maternal separation increasing rats' sensitivity to footshock (Experiment 5) and may in part be related to superior long-term memory for contexts in P17 maternally separated rats (Experiment 4). Taken together, these results suggest that early life adversity may prepare young animals to respond more cautiously toward fear signals in their environment. [ABSTRACT FROM AUTHOR]

• Children and adolescents are faster to visually search for parents than strangers. • However, a fear prime attenuates this parental orienting during childhood and adolescence. • Fear may reallocate attention toward possible danger in childhood and adolescence. Adults quickly orient toward sources of danger and deploy fight-or-flight tactics to manage threatening situations. In contrast, infants who cannot implement the safety strategies available to adults and depend heavily on caregivers for survival are more likely to turn toward familiar adults, such as their parents, to help them navigate threatening circumstances. However, work has yet to investigate how readily children and adolescents orient toward their parents in threatening or fearful contexts. The current work addressed this question using a visual search paradigm that included arrays of parents' and strangers' faces as target and distractor stimuli, preceded by a fear or neutral emotional priming procedure. Linear mixed-effects models showed that children and adolescents (N = 88, age range = 4–17 years; 42M/46F) were faster to search for the face of their parent than of a stranger. However, fear priming attenuated this effect of the parent on search times, such that children and adolescents were significantly slower to orient toward their parent in an array of strangers' faces if they were first primed with fear as opposed to a neutral video. This work indicates that fear priming may phasically interfere with parental orienting during childhood and adolescence, possibly because fear reallocates attention away from parents and toward (potentially threatening) unfamiliar people in the environment to facilitate the development of independent threat learning and coping systems. [ABSTRACT FROM AUTHOR]