Ontogeny of memory: An update on 40 years of work on infantile amnesia

Madsen, Heather B.; Kim, Jee Hyun

doi:10.1016/j.bbr.2015.07.030

Cited by 74 publications

(66 citation statements)

References 198 publications

(253 reference statements)

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“…As these authors already noticed, people tend to overestimate the age at which they learned the first-acquired words. Very few participants give ratings below the age of 3, which corresponds to the time of infantile amnesia (Madsen & Kim, 2016). Interestingly, Łuniewska et al (in press) observed that participants gave…”

Section: Methodsmentioning

confidence: 99%

Age of acquisition ratings score better on criterion validity than frequency trajectory or ratings “corrected” for frequency

Brysbaert

2017

Quarterly Journal of Experimental Psychology

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From the very first studies on the effect of age of acquisition (AoA) on word processing, researchers have validated their AoA ratings by correlating them with other, more objective indices of the age at which children know words. Still, the ratings have been questioned, and alternative measures have been proposed. Two of these are differences in word frequency between language directed at young children and language directed at older children (frequency trajectory) and AoA ratings corrected for word frequency. Surprisingly, the criterion validity of these alternative measures has never been established, partly because one of the validation criteria (the age at which children are able to name pictures) has been questioned. In the present study, four databases are used that aimed to establish the order of English word acquisition, going from the very first words learned to words taught in secondary education. The criteria for word knowledge included word production, multiple-choice questions about the meaning of the words, and teacher judgments about when words should be taught in the school curriculum. For all databases, the frequency trajectory correlated substantially less with the criterion than AoA ratings. For all but one, the same was true for AoA ratings “corrected” for other variables. On the basis of these findings, researchers should be cautious interpreting null effects with the “improved” variables as evidence against a genuine AoA effect.

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Section: Methodsmentioning

confidence: 99%

Age of acquisition ratings score better on criterion validity than frequency trajectory or ratings “corrected” for frequency

Brysbaert

2017

Quarterly Journal of Experimental Psychology

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“…And although the threats of infancy are largely buffered by parental presence (32) and the rapid forgetting of fearful events ensured by infantile amnesia for this developmental period (33), infants are frequently exposed to many forms of adversity. Such exposure is a potent risk factor for physical and mental health problems in later life [review in Ref.…”

Section: The Ravages Of Early Adversitymentioning

confidence: 99%

“…The SAH-MI in its simplest form stipulates that susceptibility to mental illness is increased by adverse experiences that occur during an early, developmentally sensitive window. This sensitive window exists in other altricial species, e.g., rats (33) and dogs (79), and corresponds in humans to the period from birth to approximately 3.5 years of age (80). It is commonly referred to as the infantile amnesia period (33, 81) and is defined more fully later.…”

Section: The Stress Acceleration Hypothesis Of Mental Illnessmentioning

confidence: 99%

“…This sensitive window exists in other altricial species, e.g., rats (33) and dogs (79), and corresponds in humans to the period from birth to approximately 3.5 years of age (80). It is commonly referred to as the infantile amnesia period (33, 81) and is defined more fully later. Early exposure to adversity is postulated to trigger a pattern of changes that is common across species, specifically, a precocious maturation of emotional regulation systems such that basic emotion processes, particularly those governing fear expression, learning and extinction for the infant, shift prematurely to an adult-like form.…”

Section: The Stress Acceleration Hypothesis Of Mental Illnessmentioning

confidence: 99%

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The Stress Acceleration Hypothesis of Nightmares

Nielsen

2017

Front. Neurol.

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Adverse childhood experiences can deleteriously affect future physical and mental health, increasing risk for many illnesses, including psychiatric problems, sleep disorders, and, according to the present hypothesis, idiopathic nightmares. Much like post-traumatic nightmares, which are triggered by trauma and lead to recurrent emotional dreaming about the trauma, idiopathic nightmares are hypothesized to originate in early adverse experiences that lead in later life to the expression of early memories and emotions in dream content. Accordingly, the objectives of this paper are to (1) review existing literature on sleep, dreaming and nightmares in relation to early adverse experiences, drawing upon both empirical studies of dreaming and nightmares and books and chapters by recognized nightmare experts and (2) propose a new approach to explaining nightmares that is based upon the Stress Acceleration Hypothesis of mental illness. The latter stipulates that susceptibility to mental illness is increased by adversity occurring during a developmentally sensitive window for emotional maturation—the infantile amnesia period—that ends around age 3½. Early adversity accelerates the neural and behavioral maturation of emotional systems governing the expression, learning, and extinction of fear memories and may afford short-term adaptive value. But it also engenders long-term dysfunctional consequences including an increased risk for nightmares. Two mechanisms are proposed: (1) disruption of infantile amnesia allows normally forgotten early childhood memories to influence later emotions, cognitions and behavior, including the common expression of threats in nightmares; (2) alterations of normal emotion regulation processes of both waking and sleep lead to increased fear sensitivity and less effective fear extinction. These changes influence an affect network previously hypothesized to regulate fear extinction during REM sleep, disruption of which leads to nightmares. This network consists of a fear circuit that includes amygdala, hippocampus, and medial prefrontal cortex and whose substantial overlap with the stress acceleration findings allows the latter to be incorporated into a wider, more developmentally coherent framework.

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“…Notably, the hippocampus undergoes a relatively long post-natal developmental period to become functionally competent in long-term memory formation and expression. In fact, contextual memories are retained long-term relatively late during development, around post-natal day 21 (PN21) in rats, and 3–5 years in humans (Callaghan, Li, & Richardson, 2014; Campbell & Spear, 1972; Hayne & Herbert, 2004; Madsen & Kim, 2016). The hippocampus also shows a parallel protracted postnatal structural and functional synapse and circuitry maturation (Cotman, Matthews, Taylor, & Lynch, 1973; Coyle & Yamamura, 1976; Crain, Cotman, Taylor, & Lynch, 1973; Wilson, 1984), suggesting that the functional competence in memory expression and structural maturation are co-dependent.…”

Section: Introductionmentioning

confidence: 99%

Developmental changes in plasticity, synaptic, glia and connectivity protein levels in rat dorsal hippocampus

Travaglia

Bisaz

Cruz

et al. 2016

Neurobiology of Learning and Memory

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Thus far the identification and functional characterization of the molecular mechanisms underlying synaptic plasticity, learning, and memory have not been particularly dissociated from the contribution of developmental changes. Brain plasticity mechanisms have been largely identified and studied using in vitro systems mainly derived from early developmental ages, yet they are considered to be general plasticity mechanisms underlying functions -such as long-term memory- that occurs in the adult brain. Although it is possible that part of the plasticity mechanisms recruited during development is then re-recruited in plasticity responses in adulthood, systematic investigations about whether and how activity-dependent molecular responses differ over development are sparse. Notably, hippocampal-dependent memories are expressed relatively late in development, and the hippocampus undergoes and extended developmental post-natal structural and functional maturation, suggesting that the molecular mechanisms underlying hippocampal neuroplasticity may actually significantly change over development. Here we quantified the relative basal expression levels of sets of plasticity, synaptic, glia and connectivity proteins in rat dorsal hippocampus, a region that is critical for the formation of long-term explicit memories, at two developmental ages, postnatal day 17 (PN17) and PN24, which correspond to a period of relative functional immaturity and maturity, respectively, and compared them to adult age. We found that the levels of numerous proteins and/or their phosphorylation, known to be critical for synaptic plasticity underlying memory formation, including immediate early genes (IEGs), kinases, transcription factors and AMPA receptor subunits, peak at PN17 when the hippocampus is not yet able to express long-term memory. It remains to be established if these changes result from developmental basal activity or infantile learning. Conversely, among all markers investigated, the phosphorylation of calcium calmodulin kinase II α (CamKII− α− and of extracellular signal-regulated kinases 2 (ERK-2), and the levels of GluA1 and GluA2 significantly increase from PN17 to PN24 and then remain similar in adulthood, thus representing correlates paralleling long-term memory expression ability.

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Ontogeny of memory: An update on 40 years of work on infantile amnesia

Cited by 74 publications

References 198 publications

Age of acquisition ratings score better on criterion validity than frequency trajectory or ratings “corrected” for frequency

Age of acquisition ratings score better on criterion validity than frequency trajectory or ratings “corrected” for frequency

The Stress Acceleration Hypothesis of Nightmares

Developmental changes in plasticity, synaptic, glia and connectivity protein levels in rat dorsal hippocampus

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