Psychosocial needs and interventions for young children with cystic fibrosis and their families.

This review summarises the experiences of young children and their families living with CF during the first five years of life following NBS diagnosis, as well as the options of psychosocial support available to them. We present strategies embedded within routine CF care that focus on prevention, screening, and intervention for psychosocial health and wellbeing that constitute essential components of multidisciplinary care in infancy and early childhood.

Investigating the disruptiveness of the sharing economy at the individual consumer level: How consumer reflexivity drives re-engagement in sharing.

The sharing economy represents an emerging technology-enabled socioeconomic system. Given its disruptive nature, the sharing economy not only challenges traditional marketing theories but also alters consumer norms and beliefs related to consumption concepts. Whether, when, and how the sharing economy transforms consumption remain important questions for managers to investigate. This study examines how sharing experiences influence consumers' critical self-reflection and shape their intentions to re-engage in sharing practices. With data collected from two surveys and four experiments (including three pretests and one main study), we show that consumers' perceived economic utility, social value, and sustainability potential in the sharing economy influence their intentions to re-engage in sharing practices, thus forming a loyal customer base. In addition, consumer reflexivity mediates this effect. We also show that past experience with business-to-consumer sharing practices moderates the proposed mediating effect. Overall, we demonstrate the disruptive impact of the sharing economy on individual consumers with meaningful managerial implications and contributions to marketing theories.

Estradiol is associated with altered cognitive and physiological responses during fear conditioning and extinction in healthy and spider phobic women.

The first-line psychological treatment for anxiety disorders is exposure therapy, which can be modeled in the laboratory using fear extinction. In healthy women, estradiol levels predict return of fear following extinction, whereas low levels are associated with greater return of fear. Investigating whether estradiol is similarly associated with extinction in clinically anxious women may provide insight to mechanisms underlying symptom relapse following exposure therapy. In the present study, women with spider phobia and healthy women participated in a 2-day fear conditioning and extinction procedure during a period of high or low estradiol levels. Skin conductance responses, shock expectancy, and valence ratings were measured throughout. Women exhibited comparable decreases in physiological arousal from conditioning to the end of extinction training on Day 1. However, compared to women with high estradiol, and irrespective of clinical status, women with low estradiol exhibited significant return of physiological arousal at extinction recall on Day 2, despite accurate ratings regarding the likelihood of shock. Low estradiol women also reported heightened threat expectancy and physiological responding during presentation of safety cues. These results may point to novel means of enhancing exposure therapy in women by timing treatment delivery during periods of higher estradiol levels. (PsycINFO Database Record

Infantile amnesia: forgotten but not gone.

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.

The elusive engram: what can infantile amnesia tell us about memory?

Revealing the engram is one of the greatest challenges in neuroscience. Many researchers focus on understanding the cellular and molecular mechanisms underlying the formation and maintenance of the engram, but an underutilized approach has been to investigate analogous processes associated with forgetting. Infant rodents present an ideal model for this purpose because they display a rapid form of non-pathological forgetting known as infantile amnesia (IA). Despite the widespread importance of this interesting phenomenon, the study of the neural bases of IA has remained largely neglected. Here, we consider what IA can tell us about memory. We argue that to understand the mechanisms underlying the engram we must also gain an appreciation of the mechanisms that drive forgetting.

From resilience to vulnerability: mechanistic insights into the effects of stress on transitions in critical period plasticity.

While early experiences are proposed to be important for the emergence of anxiety and other mental health problems, there is little empirical research examining the impact of such experiences on the development of emotional learning. Of the research that has been performed in this area, however, a complex picture has emerged in which the maturation of emotion circuits is influenced by the early experiences of the animal. For example, under typical laboratory rearing conditions infant rats rapidly forget learned fear associations (infantile amnesia) and express a form of extinction learning which is relapse-resistant (i.e., extinction in infant rats may be due to fear erasure). In contrast, adult rats exhibit very long-lasting memories of past learned fear associations, and express a form of extinction learning that is relapse-prone (i.e., the fear returns in a number of situations). However, when rats are reared under stressful conditions then they exhibit adult-like fear retention and extinction behaviors at an earlier stage of development (i.e., good retention of learned fear and relapse-prone extinction learning). In other words, under typical rearing conditions infant rats appear to be protected from exhibiting anxiety whereas after adverse rearing fear learning appears to make those infants more vulnerable to the later development of anxiety. While the effects of different experiences on infant rats' fear retention and extinction are becoming better documented, the mechanisms which mediate the early transition seen following stress remain unclear. Here we suggest that rearing stress may lead to an early maturation of the molecular and cellular signals shown to be involved in the closure of critical period plasticity in sensory modalities (e.g., maturation of GABAergic neurons, development of perineuronal nets), and speculate that these signals could be manipulated in adulthood to reopen infant forms of emotional learning (i.e., those that favor resilience).

Traces of memory: reacquisition of fear following forgetting is NMDAr-independent.

Recent research shows that while initial learning is dependent on N-methyl-D-aspartate receptors (NMDArs), relearning can be NMDAr-independent. In the present study we examined whether this switch also occurs following forgetting. The developing animal exhibits much more rapid rates of forgetting than adults, so infant rats were used. It was found that infant rats required NMDArs to learn fear (Experiment 1), and that this memory was forgotten after 14 d (Experiment 2). Despite forgetting, relearning fear did not require NMDAr activation (Experiment 3), even if it occurred in adulthood (Experiment 5). Importantly, animals only showed NMDAr-independent reacquisition if they had received paired (white noise-shock) training during conditioning and not if they received unpaired presentations of the white noise and shock (Experiment 4). In addition, this transition following forgetting was not stimulus specific as learning about a novel stimulus (i.e., light, Experiment 6) was also NMDAr-independent. However, reacquisition to a novel stimulus was NMDAr-dependent if the original fear memory was retained at the time of retraining (Experiment 7). Taken together, these results demonstrate how fear memories acquired early in life can have a long-lasting impact on later learning, even when they have been apparently forgotten (i.e., they are not expressed in the animal's overt behavior). Further, they support the idea that while memories may be forgotten, they are not gone.

Differential involvement of the medial prefrontal cortex in the expression of learned fear across development.

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.

Phosphorylation of mitogen-activated protein kinase in the medial prefrontal cortex and the amygdala following memory retrieval or forgetting in developing rats.

We examined neuronal correlates of forgetting in rats by detection of phosphorylated mitogen-activated protein kinase (pMAPK) in the medial prefrontal cortex (mPFC) and amygdala. In Experiment 1, postnatal day (P)23 and P16 rats received paired noise CS-shock US presentations. When tested immediately after conditioning, P23 and P16 rats exhibited similar levels of conditioned fear; when tested after 2 days, however, P16 rats showed poor CS-elicited freezing relative to P23 rats. In Experiment 2, P16 and P23 rats received either paired or unpaired CS-US presentations, and then were tested 48 h later. Consistent with Experiment 1, P16 rats showed forgetting whereas P23 rats exhibited good retention at test. Additionally, unpaired groups showed poor CS-elicited freezing at test. Immunohistochemistry showed that P23 and P16 rats given paired presentations exhibited significant elevation of pMAPK-immunoreactive (ir) neurons in the amygdala compared to rats given unpaired presentations. That is, MAPK phosphorylation in the amygdala tracked learning history rather than behavioral performance at test. In contrast, only the P23-paired group showed an elevated number of pMAPK-ir neurons in mPFC, indicating that MAPK phosphorylation in the mPFC tracks memory expression. Different test-perfusion intervals were employed in Experiment 3, which showed that the developmental dissociation in the pMAPK-ir neurons observed in the mPFC in Experiment 2 was not due to age differences in the rate of phosphorylation of MAPK. These findings provide initial evidence suggesting that while the mPFC is involved in memory retrieval, MAPK phosphorylation in the amygdala may be a persisting neural signature of fear memory.

Immunohistochemical analyses of long-term extinction of conditioned fear in adolescent rats.

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.