Association between spatial working memory and Re-experiencing symptoms in PTSD

Mathew, Abel S.; Lotfi, Salahadin; Bennett, Kenneth P.; Larsen, Sadie E.; Dean, Caron; Larson, Christine L.; Lee, Han-Joo

doi:10.1016/j.jbtep.2021.101714

Cited by 9 publications

(10 citation statements)

References 129 publications

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“…1F, G ). Hippocampal dysfunction is a crucial contributor to PTSD symptoms such as working memory [ 51 , 52 ]. We further evaluate the spatial working memory of these animals using the Y maze spontaneous alternation test (Y maze test).…”

Section: Resultsmentioning

confidence: 99%

Glucocorticoid-glucocorticoid receptor-HCN1 channels reduce neuronal excitability in dorsal hippocampal CA1 neurons

Kim

Lei

et al. 2022

Mol Psychiatry

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While chronic stress increases hyperpolarization-activated current (Ih) in dorsal hippocampal CA1 neurons, the underlying molecular mechanisms are entirely unknown. Following chronic social defeat stress (CSDS), susceptible mice displayed social avoidance and impaired spatial working memory, which were linked to decreased neuronal excitability, increased perisomatic hyperpolarization-activated cyclic nucleotide-gated (HCN) 1 protein expression, and elevated Ih in dorsal but not ventral CA1 neurons. In control mice, bath application of corticosterone reduced neuronal excitability, increased tetratricopeptide repeat–containing Rab8b-interacting protein (TRIP8b) and HCN1 protein expression, and elevated Ih in dorsal but not ventral CA1 region/neurons. Corticosterone-induced upregulation of functional Ih was mediated by the glucocorticoid receptor (GR), HCN channels, and the protein kinase A (PKA) but not the calcium/calmodulin-dependent protein kinase II (CaMKII) pathway. Three months after the end of CSDS, susceptible mice displayed persistent social avoidance when exposed to a novel aggressor. The sustained behavioral deficit was associated with lower neuronal excitability and higher functional Ih in dorsal CA1 neurons, both of which were unaffected by corticosterone treatment. Our findings show that corticosterone treatment mimics the pathophysiological effects of dorsal CA1 neurons/region found in susceptible mice. The aberrant expression of HCN1 protein along the somatodendritic axis of the dorsal hippocampal CA1 region might be the molecular mechanism driving susceptibility to social avoidance.

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Section: Resultsmentioning

confidence: 99%

Glucocorticoid-glucocorticoid receptor-HCN1 channels reduce neuronal excitability in dorsal hippocampal CA1 neurons

Kim

Lei

et al. 2022

Mol Psychiatry

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“…Using the four-factor PCL-M we were able to show that WM functioning was negatively related to PTSD-intrusions. Previously, it has been suggested that intrusions undermine WM because they interfere with inhibitory processes common to both emotional regulation strategies and WM (Mathew et al, 2022 ; Nejati et al, 2018 ). In the General Discussion, we interpret our findings as evidence that affective interference in PTSD is not due to impaired ability to inhibit task-irrelevant information, but due to the additional load on inhibitory processes posed by intrusive memories and emotions.…”

Section: Discussionmentioning

confidence: 99%

“…The effect can also be induced experimentally using mood induction (Ribeiro et al, 2019 ). Research shows that people diagnosed with PTSD are more likely than controls to have difficulty with emotional Stroop tasks, particularly in the presence of depression and anxiety-related distractors (Mathew et al, 2022 ).…”

Section: Introductionmentioning

confidence: 99%

“…It makes it possible to explain WM deficits in PTSD in a variety of ways and makes it difficult to pit one explanation against the other. For example, the reason for the greater vulnerability to emotional distractors in PTSD may be that intrusive re-experiencing (symptom cluster B) interferes with processes that inhibit external noise or because the intrusions themselves constitute a source of internal noise that taxes these processes (Mathew et al, 2022 ); that the cognitive effort involved in avoidance strategies (symptom cluster C) when confronting trauma-related triggers interferes with normal cognitive functioning, including WM (Mathew et al, 2022 ); that higher baseline levels of negative cognition/mood (symptom cluster D) means that ambiguous or mildly negative content will be more likely to trigger negative responses (Boffa et al, 2018 ); and/or that emotional content may be primed and thus more psychologically impactful because of one’s pre-existing levels arousal/ hypervigilance (symptom cluster E) (Litz & Keane, 1989 ). Note that these explanations are not mutually exclusive, and it is possible that they all receive empirical support.…”

Section: Introductionmentioning

confidence: 99%

“…Note that these explanations are not mutually exclusive, and it is possible that they all receive empirical support. Therefore, we argue for more research to determine how specific PTSD symptom clusters map onto to specific WM deficits (Mathew et al, 2022 ).…”

Section: Introductionmentioning

confidence: 99%

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Posttraumatic stress, visual working memory, and visual imagery in military personnel

Russell

Mussap²

2023

Curr Psychol

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Posttraumatic stress disorder (PTSD) is characterized by disruptions to cognitive functioning. Two studies were conducted to examine the relevance of military-related PTSD to two cognitive functions – visual working memory and visual imagery. Participants were military personnel who reported their PTSD diagnosis history and completed a self-administered screening tool for PTSD, the PTSD Checklist – Military Version. In Study 1, 138 personnel also completed a memory span task and a 2-back task using colored words in which Stroop interference was introduced via the semantic content of the words. In Study 2, a separate group of 211 personnel completed measures of perceived imagery vividness and spontaneous use of visual imagery. Interference effects on working memory in PTSD-diagnosed military personnel were not replicated. However, ANCOVA and structural equation modelling revealed that PTSD-intrusions were associated with poorer working memory whereas PTSD-arousal was associated with spontaneous use of visual imagery. We interpret these results as evidence that intrusive flashbacks disrupt working memory performance not by limiting memory capacity nor by interfering directly with memory functions such as inhibition, but by adding internal noise in the form of task-irrelevant memories and emotions. Visual imagery appears to be unrelated to these flashbacks but with arousal symptoms of PTSD, perhaps in the form of flashforwards about feared/anticipated threats.

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