Conditioned Physiological Reactivity and PTSD Symptoms Across the Menstrual Cycle: Anxiety Sensitivity as a Moderator

2020 ◽  
Author(s):  
Joseph Carpenter ◽  
Laura Bragdon ◽  
Suzanne L. Pineles

Objective: PTSD is often associated with heightened physiological reactivity during fear conditioning procedures, but results vary across studies. The present study examined whether anxiety sensitivity (AS), or the fear of arousal-related sensations, strengthens the relationship between PTSD symptoms and skin conductance responses (SCR) during fear conditioning and extinction. Because gonadal hormones implicated in fear learning processes fluctuate across the menstrual cycle, the stability of these relationships in women was examined in two distinct menstrual cycle phases. Method: Thirty-two trauma-exposed women with (n=16) and without PTSD (n=16) completed the Clinician-Administered PTSD Scale, Anxiety Sensitivity Inventory, and a fear conditioning and extinction paradigm during the mid-luteal (mLP) and early-follicular (eFP) menstrual cycle phases. Results: In the mLP, stronger SCR to stimuli paired with shock (CS+) during fear acquisition significantly predicted greater PTSD symptoms only when AS was high and after removing an outlier. This appeared driven by effects on Numbing and Hyperarousal symptom clusters. Other hypothesized interactions between AS and CS responses were not significant. However, in the eFP, differential SCR between the CS+ and CS- during extinction predicted significantly greater PTSD symptoms, and there was a trend for this effect being stronger as AS increased. Conclusions: Results offer preliminary evidence that high AS contributes to a stronger relationship between physiological responses during fear acquisition and PTSD symptoms, at least among women in the mLP. Further research investigating the impact of individual differences in traits such as AS on the relationship between conditioned fear responses and PTSD symptoms is warranted.

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A20-A20
Author(s):  
Anne Richards ◽  
Sabra Inslicht ◽  
J Russell Huie ◽  
Leslie Yack ◽  
Laura Straus ◽  
...  

Abstract Introduction Animal and human studies indicate that fear conditioning disrupts subsequent sleep, including REM sleep (REMS). REMS is thought to be central to fear information processing. We utilized an afternoon nap protocol to examine the effects of fear-potentiated startle (FPS), a variant of fear conditioning, on subsequent sleep integrity and REMS in trauma-exposed participants with varying levels of PTSD. We also examined the effects of changes in sleep integrity and REMS on subsequent retention and extinction of pre-sleep learning. Methods Participants (N=47) participated in 3 nap visits. The first was an adaptation nap. The second and third nap visits were counterbalanced: a stress-condition nap, during which participants underwent FPS procedures prior to a nap and assessment of retention of fear and safety signal learning and fear extinction after the nap, and a control visit during which participants had a nap opportunity without stressful procedures. Canonical correlation analysis assessed the relationship between FPS responses and change in subsequent sleep relative to a control nap, as well as the relationship between change in sleep from control to stress condition and both subsequent fear and safety learning retention, and subsequent extinction. Results Results demonstrated a relationship between fear learning and change in sleep and supported a relationship between safety signal learning and subsequent REMS, as well as differential conditioning and wake after sleep onset. Sleep did not predict measures of fear retention or extinction. PTSD symptoms did not predict fear learning or sleep measures. Conclusion These findings replicate prior work showing a relationship between safety learning and REMS, suggesting that this is a core mechanism through which stress impacts fear processing. Further research is critical to further understand this effect, and to examine how different aspects of fear learning impact different components of sleep. This study also demonstrates that nap studies can be a valuable approach for studying the stress-sleep relationship. Support (if any) VA Career Development Award to Dr. Richards (5IK2CX000871-05)


2019 ◽  
Author(s):  
Bianca Gerardo ◽  
Raquel Nunes R. M. Guiomar ◽  
Mariana Moura-Ramos ◽  
Ana Ganho-Ávila

Anxiety sensitivity (AS; the degree of fear of experiencing or imagining experiencing anxiety symptoms and its possible consequences) is associated with expression of conditioned fear responses. However, findings regarding the relationship between AS and fear acquisition indexed by skin conductance responses are rather conflicting. Here we aim to clarify this interaction. We classified 144 women that underwent fear conditioning procedures as either high-AS or low-AS. We found that high-AS participants show one of two patterns maintained over time: poor stimuli discrimination or good stimuli discrimination. This suggests that different patterns of fear acquisition potentially support the distinction between anxiety disorders.


Author(s):  
Julia Reinhard ◽  
Anna Slyschak ◽  
Miriam A. Schiele ◽  
Marta Andreatta ◽  
Katharina Kneer ◽  
...  

AbstractThe aim of the study was to investigate age-related differences in fear learning and generalization in healthy children and adolescents (n = 133), aged 8–17 years, using an aversive discriminative fear conditioning and generalization paradigm adapted from Lau et al. (2008). In the current task, participants underwent 24 trials of discriminative conditioning of two female faces with neutral facial expressions, with (CS+) or without (CS−) a 95-dB loud female scream, presented simultaneously with a fearful facial expression (US). The discriminative conditioning was followed by 72 generalization trials (12 CS+, 12 GS1, 12 GS2, 12 GS3, 12 GS4, and 12 CS−): four generalization stimuli depicting gradual morphs from CS+ to CS− in 20%-steps were created for the generalization phases. We hypothesized that generalization in children and adolescents is negatively correlated with age. The subjective ratings of valence, arousal, and US expectancy (the probability of an aversive noise following each stimulus), as well as skin conductance responses (SCRs) were measured. Repeated-measures ANOVAs on ratings and SCR amplitudes were calculated with the within-subject factors stimulus type (CS+, CS−, GS1-4) and phase (Pre-Acquisition, Acquisition 1, Acquisition 2, Generalization 1, Generalization 2). To analyze the modulatory role of age, we additionally calculated ANCOVAs considering age as covariate. Results indicated that (1) subjective and physiological responses were generally lower with increasing age irrespective to the stimulus quality, and (2) stimulus discrimination improved with increasing age paralleled by reduced overgeneralization in older individuals. Longitudinal follow-up studies are required to analyze fear generalization with regard to brain maturational aspects and clarify whether overgeneralization of conditioned fear promotes the development of anxiety disorders or vice versa.


2020 ◽  
Vol 35 (6) ◽  
pp. 923-923
Author(s):  
Walker N ◽  
Scott T ◽  
Spellman J ◽  
Rivera J ◽  
Waltzman D ◽  
...  

Abstract Objective Reviewed literature suggests that individuals with Posttraumatic Stress Disorder (PTSD) demonstrate cognitive deficits in attention, learning/memory, and executive functions. Less is known regarding the relationship between sleep disturbance and language abilities among individuals with PTSD. We hypothesized that subjective perceptions of PTSD-related sleep disturbance would impact language generativity in Veterans with PTSD. Methods 38 individuals (mean age = 46.58, SD = 13.55; 10% female) were administered a brief neurocognitive battery including measures of verbal generativity [i.e., Delis-Kaplan Executive Function System: Verbal fluency subtest], PTSD symptoms (i.e., clinically significant PTSD = > 35 on the PTSD Checklist for DSM-IV), self-report measures of sleep quality (Pittsburgh Sleep Quality Inventory; PSQI), and PTSD-related sleep disturbances (PSQI – Addendum for PTSD). All participants had a history of mild traumatic brain injury (mTBI). An analysis of covariance was used to assess the contribution of PTSD-related sleep disturbance on verbal fluency in Veterans with PTSD. Post-hoc analyses were conducted. Results Those without PTSD performed better on letter fluency than those with PTSD (p=.019). There was no significant effect of PTSD (presence or absence) on letter fluency performance after controlling for subjective sleep quality, F(1, 35) = 1.43, p = .239. Follow up analyses failed to show any associations between PTSD and other cognitive measures. Conclusions PTSD related sleep disturbance accounts for a significant portion of the variance in the relationship between PTSD and verbal generativity. Individuals with a history of mTBI and current PTSD symptoms, may have worse verbal generativity but is partially accounted for by PTSD related sleep disturbance.


Author(s):  
Andreas Frick ◽  
Johannes Björkstrand ◽  
Mark Lubberink ◽  
Allison Eriksson ◽  
Mats Fredrikson ◽  
...  

AbstractLearning which environmental cues that predict danger is crucial for survival and accomplished through Pavlovian fear conditioning. In humans and rodents alike, fear conditioning is amygdala-dependent and rests on similar neurocircuitry. Rodent studies have implicated a causative role for dopamine in the amygdala during fear memory formation, but the role of dopamine in aversive learning in humans is unclear. Here, we show dopamine release in the amygdala and striatum during fear learning in humans. Using simultaneous positron emission tomography and functional magnetic resonance imaging, we demonstrate that the amount of dopamine release is linked to strength of conditioned fear responses and linearly coupled to learning-induced activity in the amygdala. Thus, like in rodents, formation of amygdala-dependent fear memories in humans seems to be facilitated by endogenous dopamine release, supporting an evolutionary conserved neurochemical mechanism for aversive memory formation.


2019 ◽  
pp. 113-128
Author(s):  
Tina B Lonsdorf

Experimental fear conditioning and extinction represent basic forms of associative learning with considerable clinical relevance and serve as laboratory models for the development and treatment of anxiety disorders, respectively. There is considerable inter-individual variation in the ability to acquire and extinguish conditioned fear reactions as well as the return of fear and approximately one third of the variance in human fear conditioning and in the vulnerability for anxiety disorders can be attributed to genetic factors. The experimental paradigms of fear conditioning and extinction are particularly well suited for genetic association studies as these optimally investigate simple behavioral paradigms with sufficient inter-individual variability and clear heritability that elicit robust behavioral responses which are easy to measure and quantify and rely on a well-defined underlying neural circuitry. Understanding the molecular pathways that mediate conditioning and extinction might therefore make an important contribution to the study of anxiety pathophysiology and resilience. Because a significant proportion of patients do not respond to or tolerate standard treatments, such advances may ultimately open up new perspectives for pharmacological interventions (i.e. pharmacologically enhanced CBT) or the individualization of current prevention and treatment programs. In the future, translational work employing a synergy between molecular genetics, neuroimaging, psychophysiology and psychopharmacology will be powerful in unraveling the neurobiology of fear learning and extinction processes and the investigation of genetic polymorphisms in fear learning and extinction processes represents one avenue along this path.


2017 ◽  
Author(s):  
Neda Assareh ◽  
Elena E. Bagley ◽  
Pascal Carrive ◽  
Gavan P. McNally

AbstractThe midbrain periaqueductal gray (PAG) coordinates the expression and topography of defensive behaviors to threat and also plays an important role in Pavlovian fear learning itself. Whereas the role of PAG in expression of defensive behavior is well understood, the relationship between activity of PAG neurons and fear learning, the exact timing of PAG contributions to learning during the conditioning trial, and the contributions of different PAG columns to fear learning are poorly understood. We assessed the effects of optogenetic inhibition of lateral (LPAG) and ventrolateral (VLPAG) PAG neurons on fear learning. Using adenoassociated viral vectors expressing halorhodopsin (eNpHR3.0), we show that brief optogenetic inhibition of LPAG or VLPAG during delivery of the shock unconditioned stimulus (US) augments acquisition of contextual or cued fear conditioning and we also show that this inhibition augments post-encounter defensive responses to a non-noxious threat. Taken together, these results show that LPAG and VLPAG serve a key role in regulation of Pavlovian fear learning at the time of US delivery. These findings provide strong support for existing models which state that LPAG and VLPAG contribute to a fear prediction error signal determining variations in the effectiveness of the aversive US in supporting learning.


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