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The updating of a memory is triggered whenever it is reactivated and a mismatch from what is expected (i.e., prediction error) is detected, a process that can be unraveled through the memory's sensitivity to protein synthesis inhibitors (i.e., reconsolidation). As noted in previous studies, in Pavlovian threat/aversive conditioning in adult rats, prediction error detection and its associated protein synthesis-dependent reconsolidation can be triggered by reactivating the memory with the conditioned stimulus (CS), but without the unconditioned stimulus (US), or by presenting a CS-US pairing with a different CS-US interval than during the initial learning. Whether similar mechanisms underlie memory updating in the young is not known. Using similar paradigms with rapamycin (an mTORC1 inhibitor), we show that preweaning rats (PN18-20) do form a long-term memory of the CS-US interval, and detect a 10-sec versus 30-sec temporal prediction error. However, the resulting updating/reconsolidation processes become adult-like after adolescence (PN30-40). Our results thus show that while temporal prediction error detection exists in preweaning rats, specific infant-type mechanisms are at play for associative learning and memory., (© 2017 Tallot et al.; Published by Cold Spring Harbor Laboratory Press.)

Children form a strong attachment to their caregiver--even when that caretaker is abusive. Paradoxically, despite the trauma experienced within this relationship, the child develops a preference for trauma-linked cues--a phenomenon known as trauma bonding. Although infant trauma compromises neurobehavioral development, the mechanisms underlying the interaction between infant trauma bonding (i.e., learned preference for trauma cues) and the long-term effects of trauma (i.e., depressive-like behavior, amygdala dysfunction) are unknown. We modeled infant trauma bonding by using odor-shock conditioning in rat pups, which engages the attachment system and produces a life-long preference for the odor that was paired with shock. In adulthood, this trauma-linked odor rescues depressive-like behavior and amygdala dysfunction, reduces corticosterone (CORT) levels, and exerts repair-related changes at the molecular level. Amygdala microarray after rescue implicates serotonin (5-HT) and glucocorticoids (GCs), and a causal role was verified through microinfusions. Blocking amygdala 5-HT eliminates the rescue effect; increasing amygdala 5-HT and blocking systemic CORT mimics it. Our findings suggest that infant trauma cues share properties with antidepressants and safety signals and provide insight into mechanisms by which infant trauma memories remain powerful throughout life.

Although the basolateral amygdala (BLA) plays a crucial role for the acquisition of fear memories, sensory cortices are involved in their long-term storage in rats. However, the time course of their respective involvement has received little investigation. Here we assessed the role of the glutamatergic N-methyl-d-aspartate (NMDA) receptors in the BLA and olfactory cortex at discrete moments of an odor fear conditioning session. We showed that NMDA receptors in BLA are critically involved in odor fear acquisition during the first association but not during the next ones. In the cortex, NMDA receptor activation at encoding is not necessary for recent odor fear memory while its role in remote memory storage needs further investigation., (© 2014 Hegoburu et al.; Published by Cold Spring Harbor Laboratory Press.)

The aim of the present study was to investigate whether neonatal odor experience associated with the mother affects food avoidance learning and basolateral amygdala (BLA) involvement in adulthood. Odorization of mother's nipples with banana or almond solutions from birth to weaning resulted in an impairment at adulthood of conditioned odor aversion (COA). These effects were specific to the early-experienced odor since no deficit was observed for COA to a novel odor (Experiment 1). In contrast, mere exposure to an odor in the home cage instead of on mother's nipples induced no deficit in COA at adulthood (Experiment 2). Finally, transitory inactivation of the BLA during COA acquisition in adult animals impaired the normal COA of naïve animals but also the attenuated COA of rats with early odor experience on the mother (Experiment 3). These results demonstrate that neonatal odor experience associated with the mother promotes the acquisition of appetitive memories which can interfere with food avoidance learning in adulthood. They also suggest that this early experience did not modify the BLA involvement in learned aversion.

Background: Early life adverse experience alters adult emotional and cognitive development. Here we assess early life learning about adverse experience and its consequences on adult fear conditioning and amygdala activity., Methods: Neonatal rats were conditioned daily from 8-12 days-old with paired odor (conditioned stimulus, CS) .5mA shock, unpaired, odor-only, or naive (no infant conditioning). In adulthood, each infant training group was divided into three adult training groups: paired, unpaired or odor-only, using either the same infant CS odor, or a novel adult CS odor without or with the infant CS present as context. Adults were cue tested for freezing (odor in novel environment), with amygdala (14)C 2-DG autoradiography and electrophysiology assessment., Results: Infant paired odor-shock conditioning attenuated adult fear conditioning, but only if the same infant CS odor was used. The (14)C 2-DG activity correlated with infant paired odor-shock conditioning produced attenuated amygdala but heightened olfactory bulb activity. Electrophysiological amygdala assessment further suggests early experience causes changes in amygdala processing as revealed by increased paired-pulse facilitation in adulthood., Conclusions: This suggests some enduring effects of early life adversity (shock) are under CS control and dependent upon learning for their impact on later adult fear learning.

The widely used Pavlovian fear-conditioning paradigms used for studying the neurobiology of learning and memory have mainly used auditory cues as conditioned stimuli (CS). The present work assessed the neural network involved in olfactory fear conditioning, using olfactory bulb stimulation-induced field potential signal (EFP) as a marker of plasticity in the olfactory pathway. Training consisted of a single training session including six pairings of an odor CS with a mild foot-shock unconditioned stimulus (US). Twenty-four hours later, the animals were tested for retention of the CS as assessed by the amount of freezing exhibited in the presence of the learned odor. Behavioral data showed that trained animals exhibited a significantly higher level of freezing in response to the CS than control animals. In the same animals, EFPs were recorded in parallel in the anterior piriform cortex (aPC), posterior piriform cortex (pPC), cortical nucleus of the amygdala (CoA), and basolateral nucleus of the amygdala (BLA) following electrical stimulation of the olfactory bulb. Specifically, EFPs recorded before (baseline) and after (during the retention test) training revealed that trained animals exhibited a lasting increase (present before and during presentation of the CS) in EFP amplitude in CoA, which is the first amygdaloid target of olfactory information. In addition, a transient increase was observed in pPC and BLA during presentation of the CS. These data indicate that the olfactory and auditory fear-conditioning neural networks have both similarities and differences, and suggest that the fear-related behaviors in each sensory system may have at least some distinct characteristics. (Contains 2 tables and 4 figures.)

Interval timing refers to the ability to perceive, estimate and discriminate durations in the range of seconds to minutes. Very little is currently known about the ontogeny of interval timing throughout development. On the other hand, even though the neural circuit sustaining interval timing is a matter of debate, the striatum has been suggested to be an important component of the system and its maturation occurs around the third post-natal (PN) week in rats. The global aim of the present study was to investigate interval timing abilities at an age for which striatum is not yet mature. We used odor fear conditioning, as it can be applied to very young animals. In odor fear conditioning, an odor is presented to the animal and a mild footshock is delivered after a fixed interval. Adult rats have been shown to learn the temporal relationships between the odor and the shock after a few associations. The first aim of the present study was to assess the activity of the striatum during odor fear conditioning using 2-Deoxyglucose autoradiography during development in rats. The data showed that although fear learning was displayed at all tested ages, activation of the striatum was observed in adults but not in juvenile animals. Next, we assessed the presence of evidence of interval timing in ages before and after the inclusion of the striatum into the fear conditioning circuit. We used an experimental setup allowing the simultaneous recording of freezing and respiration that have been demonstrated to be sensitive to interval timing in adult rats. This enabled the detection of duration-related temporal patterns for freezing and/or respiration curves in infants as young as 12 days PN during odor fear conditioning. This suggests that infants are able to encode time durations as well as and as quickly as adults while their striatum is not yet functional. Alternative networks possibly sustaining interval timing in infant rats are discussed. [ABSTRACT FROM AUTHOR]

• Subjective experiences are valuable for analyzing fear and fear-related memories. • Autobiographies are valuable for analyzing fear and fear-related memories. • These analyses would be valuable for longitudinal analyses in individuals. • These analyses would be valuable to measure response to behavioral and/or pharmacological interventions. • Linguistic analysis should be further developed and incorporated into standard care. Fear is an emotion that serves as a driving factor in how organisms move through the world. In this review, we discuss the current understandings of the subjective experience of fear and the related biological processes involved in fear learning and memory. We first provide an overview of fear learning and memory in humans and animal models, encompassing the neurocircuitry and molecular mechanisms, the influence of genetic and environmental factors, and how fear learning paradigms have contributed to treatments for fear-related disorders, such as posttraumatic stress disorder. Current treatments as well as novel strategies, such as targeting the perisynaptic environment and use of virtual reality, are addressed. We review research on the subjective experience of fear and the role of autobiographical memory in fear-related disorders. We also discuss the gaps in our understanding of fear learning and memory, and the degree of consensus in the field. Lastly, the development of linguistic tools for assessments and treatment of fear learning and memory disorders is discussed. [ABSTRACT FROM AUTHOR]

Recent evidence indicates that reactivation of consolidated memories returns them to a protein-synthesis-dependent state called reconsolidation. The hypothesis that memories reconsolidate has never been assessed in social memory. The authors tested whether sheep (Ovis aries) mothers' memory of their lambs undergoes reconsolidation upon reactivation. After 7 days of mother-young contact, ewes were separated from their lambs for 8 hr, after which the lambs were reintroduced to their mothers for a 10-min reactivation session. Before reactivation, mothers received a subcutaneous injection of either the protein-synthesis inhibitor cycloheximide (CY, 1 mg/kg) or vehicle. Mothers' lamb memory was tested 1 hr (short-term memory [STM]) or 16 hr (long-term memory [LTM]) after reactivation. Mothers treated with CY exhibited intact STM but deficient LTM. CY injection without reactivation or before presentation of an alien lamb induced no deficit in LTM. CY-induced LTM deficit was alleviated by (a) introducing a reminder just before the LTM test, (b) extending mother-young contact, and (c) preventing suckling by the familiar lamb during reactivation. Thus, reconsolidation can be shown to exist in social memory, and some of its boundary conditions are discussed. [ABSTRACT FROM AUTHOR]