Selectively Interfering With Intrusive but Not Voluntary Memories of a Trauma Film: Accounting for the Role of Associative Memory.

Intrusive memories of a traumatic event can be reduced by a subsequent interference procedure, seemingly sparing voluntary memory for that event. This selective-interference effect has potential therapeutic benefits (e.g., for emotional disorders) and legal importance (e.g., for witness testimony). However, the measurements of intrusive memory and voluntary memory typically differ in the role of associations between a cue and the emotional memory "hotspots." To test this, we asked participants to watch a traumatic film followed by either an interference procedure (reminder plus Tetris) or control procedure (reminder only). Measurement of intrusions (using a laboratory task) and voluntary memory (recognition for film stills) were crossed with the presence or absence of associative cues. The reminder-plus-Tetris group exhibited fewer intrusions despite comparable recognition memory, replicating the results of prior studies. Note that this selective interference did not appear to depend on associative cues. This involuntary versus voluntary memory dissociation for emotional material further supports separate-trace memory theories and has applied advantages

Playing the computer game Tetris prior to viewing traumatic film material and subsequent intrusive memories: Examining proactive interference.

Visuospatial working memory (WM) tasks performed concurrently or after an experimental trauma (traumatic film viewing) have been shown to reduce subsequent intrusive memories (concurrent or retroactive interference, respectively). This effect is thought to arise because, during the time window of memory consolidation, the film memory is labile and vulnerable to interference by the WM task. However, it is not known whether tasks before an experimental trauma (i.e. proactive interference) would also be effective. Therefore, we tested if a visuospatial WM task given before a traumatic film reduced intrusions. Findings are relevant to the development of preventative strategies to reduce intrusive memories of trauma for groups who are routinely exposed to trauma (e.g. emergency services personnel) and for whom tasks prior to trauma exposure might be beneficial. Participants were randomly assigned to 1 of 2 conditions. In the Tetris condition (n = 28), participants engaged in the computer game for 11 min immediately before viewing a 12-min traumatic film, whereas those in the Control condition (n = 28) had no task during this period. Intrusive memory frequency was assessed using an intrusion diary over 1-week and an Intrusion Provocation Task at 1-week follow-up. Recognition memory for the film was also assessed at 1-week. Compared to the Control condition, participants in the Tetris condition did not report statistically significant difference in intrusive memories of the trauma film on either measure. There was also no statistically significant difference in recognition memory scores between conditions. The study used an experimental trauma paradigm and findings may not be generalizable to a clinical population. Compared to control, playing Tetris before viewing a trauma film did not lead to a statistically significant reduction in the frequency of later intrusive memories of the film. It is unlikely that proactive interference, at least with this task, effectively influences intrusive memory development. WM tasks administered during or after trauma stimuli, rather than proactively, may be a better focus for intrusive memory amelioration

Multiple memory systems, multiple time points: how science can inform treatment to control the expression of unwanted emotional memories.

Memories that have strong emotions associated with them are particularly resilient to forgetting. This is not necessarily problematic, however some aspects of memory can be. In particular, the involuntary expression of those memories, e.g. intrusive memories after trauma, are core to certain psychological disorders. Since the beginning of this century, research using animal models shows that it is possible to change the underlying memory, for example by interfering with its consolidation or reconsolidation. While the idea of targeting maladaptive memories is promising for the treatment of stress and anxiety disorders, a direct application of the procedures used in non-human animals to humans in clinical settings is not straightforward. In translational research, more attention needs to be paid to specifying what aspect of memory (i) can be modified and (ii) should be modified. This requires a clear conceptualization of what aspect of memory is being targeted, and how different memory expressions may map onto clinical symptoms. Furthermore, memory processes are dynamic, so procedural details concerning timing are crucial when implementing a treatment and when assessing its effectiveness. To target emotional memory in its full complexity, including its malleability, science cannot rely on a single method, species or paradigm. Rather, a constructive dialogue is needed between multiple levels of research, all the way 'from mice to mental health'.This article is part of a discussion meeting issue 'Of mice and mental health: facilitating dialogue between basic and clinical neuroscientists'.We are grateful to the Royal Society for their support of the costs of attending this meeting ‘Of mice and mental health: facilitating dialogue between basic and clinical neuroscientists' convened by Amy L. Milton and Emily A. Holmes. R.M.V. is supported by the European Union's Horizon 2020 research and innovation programme under grant agreement no. 705641 (SUAI/023/RG92025). A.L.-Z. was supported by a Cambridge International Scholarship awarded by the Cambridge Commonwealth, European and International Trust. R.N.H. is supported by the UK Medical Research Council Programme (SUAI/010/ RG91365). E.A.H. receives support from the Karolinska Institutet and the Lupina Foundation. Funding to pay the Open Access publication charges for this article was provided by the UK Medical Research Council (SUAI/013/ RG91365)

The trauma film paradigm as an experimental psychopathology model of psychological trauma: intrusive memories and beyond

A better understanding of psychological trauma is fundamental to clinical psychology. Following traumatic event(s), a clinically significant number of people develop symptoms, including those of Acute Stress Disorder and/or Post Traumatic Stress Disorder. The trauma film paradigm offers an experimental psychopathology model to study both exposure and reactions to psychological trauma, including the hallmark symptom of intrusive memories. We reviewed 74 articles that have used this paradigm since the earliest review (Holmes & Bourne, 2008) until July 2014. Highlighting the different stages of trauma processing, i.e. pre-, peri- and post-trauma, the studies are divided according to manipulations before, during and after film viewing, for experimental as well as correlational designs. While the majority of studies focussed on the frequency of intrusive memories, other reactions to trauma were also modelled. We discuss the strengths and weaknesses of the trauma film paradigm as an experimental psychopathology model of trauma, consider ethical issues, and suggest future directions. By understanding the basic mechanisms underlying trauma symptom development, we can begin to translate findings from the laboratory to the clinic, test innovative science-driven interventions, and in the future reduce the debilitating effects of psychopathology following stressful and/or traumatic events

Iconicity emerges and is maintained in spoken language

Iconicity is the property whereby signs (vocal or manual) resemble their referents. Iconic signs are easy to relate to the world, facilitating learning and processing. In this study, we examined whether the benefits of iconicity would lead to its emergence and to maintenance in language. We focused on shape iconicity (the association between rounded objects and round-sounding words like “bouba” and between spiky objects and spiky-sounding words like “kiki”) and motion iconicity (the association between longer words and longer events). In Experiment 1, participants generated novel labels for round versus spiky shapes and long versus short movements (Experiment 1a: text, Experiment 1b: speech). Labels for each kind of stimulus differed in a way that was consistent with previous studies of iconicity. This suggests that iconicity emerges even on a completely unconstrainted task. In Experiment 2 (Experiment 2a: text, Experiment 2b: speech), we simulated language change in the laboratory (as iterated learning) and found that both forms of iconicity were introduced and maintained through generations of language users. Thus, we demonstrate the emergence of iconicity in spoken languages, and we argue that these results reflect a pressure for language systems to be referential, which favors iconic forms in the cultural evolution of language (at least up to a point where it is balanced by other pressures, e.g., discriminability). This can explain why we have iconicity across natural languages and may have implications for debates on language origins. (PsycInfo Database Record (c) 2021 APA, all rights reserved

An H4K16 histone acetyltransferase mediates decondensation of the X chromosome in C. elegans males

Abstract Background In C. elegans, in order to equalize gene expression between the sexes and balance X and autosomal expression, two steps are believed to be required. First, an unknown mechanism is hypothesized to upregulate the X chromosome in both sexes. This mechanism balances the X to autosomal expression in males, but creates X overexpression in hermaphrodites. Therefore, to restore the balance, hermaphrodites downregulate gene expression twofold on both X chromosomes. While many studies have focused on X chromosome downregulation, the mechanism of X upregulation is not known. Results To gain more insight into X upregulation, we studied the effects of chromatin condensation and histone acetylation on gene expression levels in male C. elegans. We have found that the H4K16 histone acetyltransferase MYS-1/Tip60 mediates dramatic decondensation of the male X chromosome as measured by FISH. However, RNA-seq analysis revealed that MYS-1 contributes only slightly to upregulation of gene expression on the X chromosome. These results suggest that the level of chromosome decondensation does not necessarily correlate with the degree of gene expression change in vivo. Furthermore, the X chromosome is more sensitive to MYS-1-mediated decondensation than the autosomes, despite similar levels of H4K16ac on all chromosomes, as measured by ChIP-seq. H4K16ac levels weakly correlate with gene expression levels on both the X and the autosomes, but highly expressed genes on the X chromosome do not contain exceptionally high levels of H4K16ac. Conclusion These results indicate that H4K16ac and chromosome decondensation influence regulation of the male X chromosome; however, they do not fully account for the high levels of gene expression observed on the X chromosomes.http://deepblue.lib.umich.edu/bitstream/2027.42/134665/1/13072_2016_Article_97.pd

Selectively Interfering With Intrusive but Not Voluntary Memories of a Trauma Film: Accounting for the Role of Associative Memory

Intrusive memories of a traumatic event can be reduced by a subsequent interference procedure, seemingly sparing voluntary memory for that event. This selective-interference effect has potential therapeutic benefits (e.g., for emotional disorders) and legal importance (e.g., for witness testimony). However, the measurements of intrusive memory and voluntary memory typically differ in the role of associations between a cue and the emotional memory “hotspots.” To test this, we asked participants to watch a traumatic film followed by either an interference procedure (reminder plus Tetris) or control procedure (reminder only). Measurement of intrusions (using a laboratory task) and voluntary memory (recognition for film stills) were crossed with the presence or absence of associative cues. The reminder-plus-Tetris group exhibited fewer intrusions despite comparable recognition memory, replicating the results of prior studies. Note that this selective interference did not appear to depend on associative cues. This involuntary versus voluntary memory dissociation for emotional material further supports separate-trace memory theories and has applied advantages

The Anti-Sigma Factor MucA of Pseudomonas aeruginosa: Dramatic Differences of a mucA22 vs. a ΔmucA Mutant in Anaerobic Acidified Nitrite Sensitivity of Planktonic and Biofilm Bacteria in vitro and During Chronic Murine Lung Infection

Mucoid mucA22 Pseudomonas aeruginosa (PA) is an opportunistic lung pathogen of cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD) patients that is highly sensitive to acidified nitrite (A-NO2-). In this study, we first screened PA mutant strains for sensitivity or resistance to 20 mM A-NO2- under anaerobic conditions that represent the chronic stages of the aforementioned diseases. Mutants found to be sensitive to A-NO2- included PA0964 (pmpR, PQS biosynthesis), PA4455 (probable ABC transporter permease), katA (major catalase, KatA) and rhlR (quorum sensing regulator). In contrast, mutants lacking PA0450 (a putative phosphate transporter) and PA1505 (moaA2) were A-NO2- resistant. However, we were puzzled when we discovered that mucA22 mutant bacteria, a frequently isolated mucA allele in CF and to a lesser extent COPD, were more sensitive to A-NO2- than a truncated ΔmucA deletion (Δ157–194) mutant in planktonic and biofilm culture, as well as during a chronic murine lung infection. Subsequent transcriptional profiling of anaerobic, A-NO2--treated bacteria revealed restoration of near wild-type transcript levels of protective NO2- and nitric oxide (NO) reductase (nirS and norCB, respectively) in the ΔmucA mutant in contrast to extremely low levels in the A-NO2--sensitive mucA22 mutant. Proteins that were S-nitrosylated by NO derived from A-NO2- reduction in the sensitive mucA22 strain were those involved in anaerobic respiration (NirQ, NirS), pyruvate fermentation (UspK), global gene regulation (Vfr), the TCA cycle (succinate dehydrogenase, SdhB) and several double mutants were even more sensitive to A-NO2-. Bioinformatic-based data point to future studies designed to elucidate potential cellular binding partners for MucA and MucA22. Given that A-NO2- is a potentially viable treatment strategy to combat PA and other infections, this study offers novel developments as to how clinicians might better treat problematic PA infections in COPD and CF airway diseases