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Recent studies have shown that exposure to a novel environment may stabilize the persistence of weak memories, a phenomenon often attributed to a process referred to as "behavioral tagging." While this phenomenon has been repeatedly demonstrated in adult animals, no studies to date have examined whether it occurs in infant animals, which is surprising given that infants exhibit an impaired ability to form long-term memories (LTMs). In the present study, infant (i.e., postnatal day (P) 17) rats were placed in a context and repeatedly shocked. Infant rats given brief open field exposure 1 h, but not 2 h, prior to conditioning exhibited enhanced retention when tested 1 d later (Experiments 1 and 2), but comparable retention when tested shortly after training (Experiment 2). Thus, exploration of an open field facilitates subsequent context fear memories by enhancing the persistence of the memory rather than strengthening the context-shock association at encoding. While exploration of an open field did not lead to better memory when animals were tested 3 d later (Experiment 3), a brief pretest shock led to a more pronounced reinstatement effect in rats exposed to the open field 1 h before conditioning (Experiment 4). Finally, unlike what has been reported in adults, Experiments 5 and 6 suggest that familiarization of the open field before subsequent exposure does not abolish the behavioral tagging effect in infants. Overall, while these findings suggest that similar behavioral tagging mechanisms to those reported in adults might be involved in the formation of LTMs in infant rats, they also suggest that there may be developmental differences in the retention of familiarization experiences.

NMDA receptors (NMDARs) are considered critical for the consolidation of extinction but recent work challenges this assumption. Namely, NMDARs are not required for extinction retention in infant rats as well as when extinction training occurs for a second time (i.e., reextinction) in adult rats. In this study, a possible third instance of NMDAR-independent extinction was tested. Although adolescents typically exhibit impaired extinction retention, rats that are conditioned as juveniles and then given extinction training as adolescents (JuvCond-AdolesExt) have good extinction retention. Unexpectedly, this good extinction retention is not associated with an up-regulation of a synaptic plasticity marker in the medial prefrontal cortex, a region implicated in extinction consolidation. In the current study, rats received either the noncompetitive NMDAR antagonist MK801 (0.1 mg/kg, s.c.) or saline before extinction training. In several experiments, rats conditioned and extinguished as juveniles, adolescents, or adults exhibited impaired extinction retention after MK801 compared to saline, but this effect was not observed in JuvCond-AdolesExt rats. Further experiments ruled out several alternative explanations for why NMDAR antagonism did not affect extinction retention in adolescents extinguishing fear learned as a juvenile. These results illustrate yet another circumstance in which NMDARs are not required for successful extinction retention and highlight the complexity of fear inhibition across development.

This article presents a commentary on Sen and Gredebäck’s “Methodological integrity assessment in the mobile paradigm literature: A lesson for understanding opportunistic use of researcher degrees of freedom in psychology” presented in this issue. The authors discuss the operant mobile paradigm in infant memory research as well as degrees of freedom and an evaluation of the paper’s simulation analyses.

There is growing appreciation for the substantial individual differences in the acquisition and inhibition of aversive associations, and the insights this might give into identifying individuals particularly vulnerable to stress and psychopathology. We examined whether animals that differed in rate of extinction (i.e., Fast versus Slow) were different in their response to an acute stress in adulthood or following a chronic stress that occurred either early or later in life. We found that Slow Extinguishers had significantly poorer extinction retention than Fast Extinguishers, but an acute stressor did not differentially affect anxiety-like behavior in the two groups. Further, while exposure to chronic stress in adulthood did not impact on the extinction phenotypes or anxiety-like behavior, exposure to chronic stress early in life affected both extinction retention and anxiety-like behavior. These findings have implications for the development of a more nuanced approach to identifying those most at risk of anxiety disorders.

These experiments examined the relationship between the neurotrophic factor fibroblast growth factor 2 (FGF2) and individual differences in the expression of conditioned fear. Experiments 1 and 2 demonstrated that rats naturally expressing low levels of contextual or cued fear have higher levels of hippocampal FGF2 relative to rats that express high levels of conditioned fear and nonconditioned rats. Experiment 3 demonstrated that hippocampal FGF2 is not increased in rats that exhibit pharmacological-induced amnesia of conditioned fear. Together, these experiments provide evidence that FGF2 may be an endogenous regulator of fear responses to conditioned stimuli.

Fear inhibition is markedly impaired in adolescent rodents and humans. The present experiments investigated whether this impairment is critically determined by the animal's age at the time of fear learning or their age at fear extinction. Male rats (n = 170) were tested for extinction retention after conditioning and extinction at different ages. We examined neural correlates of impaired extinction retention by detection of phosphorylated mitogen-activated protein kinase immunoreactivity (pMAPK-IR) in several brain regions. Unexpectedly, adolescent rats exhibited good extinction retention if fear was acquired before adolescence. Further, fear acquired in adolescence could be successfully extinguished in adulthood but not within adolescence. Adolescent rats did not show extinction-induced increases in pMAPK-IR in the medial prefrontal cortex or the basolateral amygdala, or a pattern of reduced caudal central amygdala pMAPK-IR, as was observed in juveniles. This dampened prefrontal and basolateral amygdala MAPK activation following extinction in adolescence occurred even when there was no impairment in extinction retention. In contrast, only adolescent animals that exhibited impaired extinction retention showed elevated pMAPK-IR in the posterior paraventricular thalamus. These data suggest that neither the animal's age at the time of fear acquisition or extinction determines whether impaired extinction retention is exhibited. Rather, it appears that forming competing fear conditioning and extinction memories in adolescence renders this a vulnerable developmental period in which fear is difficult to inhibit. Furthermore, even under conditions that promote good extinction, the neural correlates of extinction in adolescence are different than those recruited in animals of other ages.

This study examined how adventure educators could use systematic feedback to improve their teaching skills. Evaluative instruments demonstrated a statistically significant improvement in teaching skills when applied at an outdoor education center in Western Canada. Concurrent focus group interviews enabled instructors to reflect on student feedback to improve teaching in subsequent courses. Instructors had the opportunity to share their experiences, thereby solidifying their learning and validating their practices. The triangulation of quantitative and qualitative data yielded a descriptive model of the reflective process, featuring multiple channels for repeated, systematic feedback to promote continuous reflection. Creating group opportunities for adventure educators to share their teaching experiences is recommended to facilitate instructional improvement, boost staff morale, and instill a sense of professionalism.

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.

Adolescent rats exhibit impaired extinction retention compared to pre-adolescent and adult rats. A single nonreinforced exposure to the conditioned stimulus (CS; a retrieval trial) given shortly before extinction has been shown in some circumstances to reduce the recovery of fear after extinction in adult animals. This study investigated whether a retrieval-extinction procedure would reduce the recovery of extinguished fear in adolescent rats. Furthermore, the effect of the retrieval-extinction sequence on fear recovery was examined by presenting the retrieval trial following extinction to some animals. In Experiment 1 adolescent rats received one nonreinforced CS presentation (a retrieval trial) or equivalent context exposure (no retrieval) 10 min before fear extinction. A retrieval trial shortly before extinction reduced overall levels of fear in both test contexts (i.e., it improved extinction retention and reduced renewal). In Experiment 2 a weakening of renewal was observed with a retrieval-extinction manipulation, regardless of whether the retrieval trial occurred in the training or extinction context. A key result was that a retrieval trial 10 min, but not 6 h, "after" extinction led to reduced overall levels of fear similar to that observed if the retrieval trial was given before extinction (Experiments 3 and 4), inconsistent with the current interpretation of the reduction in relapse being due to a disruption of reconsolidation. Together, these findings show that the impaired extinction retention observed in adolescents can be ameliorated by a very simple behavioral manipulation, but also raise some questions about the mechanisms underlying the retrieval-extinction effect.

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.

The aim of this study was to examine associations between ostracism, internalising problems, and threat to primary needs (belonging, control, self-esteem, meaningful existence) in children (N= 165, M age = 9 years). Ostracism was simulated experimentally using the Cyberball paradigm--a computer-based ball-throwing game--and threats to primary needs were indexed using a modified version of the primary needs questionnaire (PNQ-C; Hawes et al., 2012). Overall, children with greater internalising problems reported greater need-threat following Cyberball. Importantly however, in the domain of "belonging", the relationship between internalising problems and need-threat was moderated by inclusionary status. Specifically, children with high levels of internalising problems exhibited greater need-threat than children low in internalising problems when included by peers; yet following ostracism, children with high internalising problems were no longer distinguishable from those with low internalising problems in terms of threat to belonging.

The NMDA receptor partial agonist d-cycloserine (DCS) enhances the extinction of learned fear in rats and exposure therapy in humans with anxiety disorders. Despite these benefits, little is known about the mechanisms by which DCS promotes the loss of fear. The present study examined whether DCS augments extinction retention (1) through reductions in conditioned stimulus (CS) processing or (2) by promoting the development of conditioned inhibition to contextual cues. Rats administered DCS prior to extinction showed enhanced long-term extinction retention (Experiments 3 and 4). The same nonreinforced CS procedure used in extinction also reduced freezing at test when presented as pre-exposure before conditioning, demonstrating latent inhibition (Experiment 1). DCS administered shortly prior to pre-exposure had no effect on latent inhibition using parameters which produced weak (Experiment 2) or strong (Experiment 3) expression of latent inhibition. Therefore, DCS facilitated learning involving CS-alone exposures, but only when these exposures occurred after (extinction) and not before (latent inhibition) conditioning. We also used a retardation test procedure to examine whether the extinction context gained inhibitory properties for rats given DCS prior to extinction. With three different footshock intensities, there was no evidence that DCS promoted accrual of associative inhibition to the extinction context (Experiment 4). The present findings demonstrate that DCS does not facilitate extinction by reducing CS processing or causing the extinction context to become a conditioned inhibitor. Investigations into the mechanisms underlying the augmentation of extinction by DCS are valuable for understanding how fear can be inhibited.

Six experiments used a within-subjects renewal design to examine the involvement of kappa opioid receptors (KORs) in regulating the expression and recovery of extinguished fear. Rats were trained to fear a tone conditioned stimulus (CS) via pairings with foot shock in a distinctive context (A). This was followed by extinction training of the CS in a second context (B). Finally, all rats were tested for fear to the tone in the extinction context (ABB) and the training (ABA) or a novel (ABC) context. Intracerebroventricular (ICV) infusion of the KOR antagonist nor-binaltorphimine dihydrochloride (nor-BNI) dose-dependently prevented ABA renewal of fear, but had no effect on the expression of ABC renewal, the expression of extinction, or the expression of nonextinguished fear. Conversely, pretest infusion of the KOR agonist U50,488 hydrochloride (U50,488) selectively facilitated the expression of ABA renewal and had no effect on the expression of extinction. Pretest infusion of nor-BNI had no effect on the expression of context-specific latent inhibition. Collectively, these results suggest that KORs gate the expression of fear following extinction training and may comprise a critical neuropeptide component of the circuitry underlying context-dependent expression of fear.

These experiments examined the effects of the NMDA-receptor (NMDAr) antagonist MK801 on reacquisition and re-extinction of a conditioned fear that had been previously extinguished before injection of fibroblast growth factor-2 (FGF2) or vehicle. Recent findings have shown that relearning and re-extinction, unlike initial learning and extinction, do not depend on NMDAr activation. Three experiments demonstrated that FGF2 prevents the switch from NMDAr-dependent to NMDAr-independent reacquisition and re-extinction, suggesting that FGF2 may lead to the partial erasure of the original fear memory. These findings add to a growing body of work suggesting that FGF2 may be a novel pharmacological enhancer of exposure therapy for humans with anxiety disorders.

We compared the effect of D-cycloserine (DCS) on immediate (10 min after conditioning) and delayed (24 h after conditioning) extinction of learned fear in rats. DCS facilitated both immediate and delayed extinction when the drug was administered after extinction training. However, DCS did not facilitate immediate extinction when administered prior to extinction training (i.e., when the interval between drug administration and shock was reduced). In addition, administering five, but not two, shocks prior to extinction training disrupted the facilitating effects of DCS on delayed extinction. These results suggest that aversive experiences prior to DCS administration can prevent it from facilitating extinction.

Several recent studies report that neurotransmitters that are critically involved in extinction in adult rats are not important for extinction in young rats. Specifically, pretest injection of the [gamma]-aminobutryic acid (GABA) receptor inverse agonist FG7142 has no effect on extinction in postnatal day (P)17 rats, although it reverses extinction in P24 rats as reported by Kim and Richardson in an earlier paper. Further, pre-extinction injection of the N-methyl-d-aspartate (NMDA) receptor antagonist MK-801 has no effect on extinction in P17 rats, whereas it impairs long-term extinction in P24 rats as per Langton and colleagues in an earlier work. These findings indicate that extinction in P17 rats is qualitatively different from extinction in older rats. The present study examines the involvement of the endogenous opioid system in extinction in the developing rat using systemic injections of the [mu]-opioid receptor antagonist naloxone. Experiment 1 showed that injection of naloxone before extinction training disrupted the acquisition of extinction in both P17 and P24 rats. This effect was dependent on central rather than peripheral [mu]-opioid receptors (Experiment 2), and neither pre-test nor post-extinction injection of naloxone had effects on extinction (Experiments 3 and 4). Taken together, these findings indicate that opioid neurotransmission, in contrast to GABA and NMDA activity, is critical for extinction acquisition across development. (Contains 4 figures and 1 table.)

Four experiments studied the role of GABA[subscript A] receptors in the temporal dynamics of memory retention. Memory for an active avoidance response was a nonmonotonic function of the retention interval. When rats were tested shortly (2 min) or some time (24 h) after training, retention was excellent, but when they were tested at intermediate intervals (1-4 h), retention was poor. Activity at GABA[subscript A] receptors was critical for impairing memory retention at the intermediate intervals because injection of the GABA[subscript A] receptor partial inverse agonist FG7142 prior to test significantly improved performance. These retention enhancing effects of FG7142 were dose-dependent and not due to any nonspecific effects of FG7142 on activity. Our results suggest that the temporal dynamics of memory retention may be caused by variations in neurotransmission through the GABA[subscript A] receptor in the post-training period.