Amnesia for early life stress does not preclude the adult development of posttraumatic stress disorder symptoms in rats
Open accessAbstract
Background Traumatic experience can result in life-long changes in the ability to cope with future stressors and emotionally salient events. These experiences, particularly during early development, are a significant risk factor for later life anxiety disorders such as posttraumatic stress disorder (PTSD). However, because traumatic experience typically results in strong episodic memories, it is not known whether such long-term memories are necessary for particular features of PTSD, such as enhanced fear and anxiety. Here, we used a fear conditioning procedure in juvenile rats before maturation of the neural systems supporting declarative memory to assess the necessity of early memory to the later life development of PTSD-related symptoms.Methods Nineteen-day old rats were exposed to unpredictable and inescapable footshocks, and fear memory for the shock context was assessed during adulthood. Thereafter, adult animals were either exposed to single-trial fear conditioning or elevated plus maze or sacrificed for basal diurnal corticosterone and quantification of neuronal glucocorticoid and neuropeptide Y receptors.Results Early trauma exposed rats displayed stereotypic footshock reactivity, yet by adulthood, hippocampus-dependent contextual fear-related memory was absent. However, adult rats showed sensitized fear learning, aberrant basal circadian fluctuations of corticosterone, increased amygdalar glucocorticoid receptors, decreased time spent in the open arm of an elevated plus maze, and an odor aversion associated with early-life footshocks.Conclusions These results suggest that traumatic experience during developmental periods of hippocampal immaturity can promote lifelong changes in symptoms and neuropathology associated with human PTSD, even if there is no explicit memory of the early trauma.
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The neurocircuitry of fear learning was altered even though the learning originating in the infantile amnesia period was forgotten.
“Again, the neurocircuitry of fear learning was altered even though the learning originating in the infantile amnesia period was forgotten.”
From The Stress Acceleration Hypothesis of Nightmares (2017) · cites this paper as [147]
The Discussion reports that rats exposed to fear conditioning at postnatal day 19 lacked a lasting contextual fear memory as adults but showed heightened fear conditioning after a new shock. The Results (Experiment 4) also report increased glucocorticoid-receptor levels in the amygdala, a fear-related brain region. The claim is broader than these findings: the paper does not show that all early learning was forgotten or directly establish an alteration of fear-learning circuitry as a whole. (LLM, conf=0.82)
Experimental — accuracy not yet measuredIn the Poulos et al. study, persistence of the infantile trace was accompanied by increased expression of amygdala glucocorticoid receptors and atypical (2-peak) circadian rhythms of basal corticosterone.
“Similarly, in the Poulos et al.’s (147) study, persistence of the infantile trace was accompanied by increased expression of amygdala glucocorticoid receptors and atypical (2-peak) circadian rhythms of basal corticosterone.”
From The Stress Acceleration Hypothesis of Nightmares (2017) · cites this paper as [147]
The Results sections for Experiments 3 and 4 report a double-peaked basal corticosterone profile and increased amygdala glucocorticoid receptors in rats exposed to early-life footshocks. But the Discussion says those rats failed to show a lasting contextual fear memory in adulthood, so describing these changes as accompanying persistence of the infantile trace is not supported. (LLM, conf=0.90)
Experimental — accuracy not yet measuredInfant rats exposed to inescapable shock in one multisensory context did not fear that context as adults but did express stronger fear learning to a different context.
“In a second study (147), infant rats exposed to inescapable shock in one multisensory context did not fear that context as adults but did express stronger fear learning to a different context.”
From The Stress Acceleration Hypothesis of Nightmares (2017) · cites this paper as [147]
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References 44 · Cited by 73
- Authors
- Poulos, A. M., Reger, M., Mehta, N., Zhuravka, I., Sterlace, S. S., Gannam, C., Hovda, D. A., Giza, C. C., & Fanselow, M. S.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Poulos, Andrew M.
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2014-08
- Volume
- 76
- Issue
- 4
- Pages
- 306-314
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC3984614
- OpenAlex
- W1983196716
- Cited by
- 73
- References
- 44
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 7 · 2023: 3 · 2022: 6 · 2021: 4 · 2020: 3 · 2019: 10 · 2018: 7 · 2017: 9 · 2016: 7 · 2015: 6 · 2014: 4
- FWCI
- 6.30
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institute of Mental Health (MH 62122, MH 60093)
- Topics
- Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- post-traumatic stress disorder, early life stress, amnesia, fear conditioning, contextual fear memory, hippocampal development, glucocorticoid receptor, neuropeptide Y receptors, corticosterone, anxiety, odor aversion, footshock, rats
- MeSH terms
- Aging, Amnesia, Animals, Avoidance Learning, Brain, Conditioning, Psychological, Corticosterone, Electroshock, Exploratory Behavior, Fear, Male, Memory, Receptors, Glucocorticoid, Stress Disorders, Post-Traumatic, Stress, Psychological, Photoperiod, Receptors, Neuropeptide, Rats, Long-Evans, Uncertainty, Receptors, G-Protein-Coupled, Freezing Reaction, Cataleptic, Olfactory Perception
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