Studies using fear-conditioning paradigms have found that anxiety patients are more conditionable than individuals without these disorders, but these effects have been demonstrated inconsistently. It is unclear whether these findings have etiological significance, or whether enhanced conditionability is linked only to certain anxiety characteristics. To further examine these issues, we assessed the predictive significance of relevant subsyndromal characteristics in 72 healthy adults, including measures of worry, avoidance, anxious mood, depressed mood, and fears of anxiety symptoms (anxiety sensitivity), as well as the dimensions of neuroticism and extraversion. Of these variables, we found that the combination of higher levels of subsyndromal worry and lower levels of behavioral avoidance predicted heightened conditionability, raising questions about the etiological significance of these variables in the acquisition or maintenance of anxiety disorders. In contrast, we found that anxiety sensitivity was more linked to individual differences in orienting response than differences in conditioning per se. KeywordsFear conditioning; etiology; worry; avoidance; anxiety sensitivity; psychophysiology Prediction of "Fear" Acquisition in Healthy Control Participants in a De Novo Fear-Conditioning ParadigmDifferences in fear conditionability-the ease by which new fear associations are learned or maintained-is a potential etiological factor for the development of anxiety disorders. Individuals who easily acquire fears to negative stimuli might be at greater risk for developing anxiety disorders in response to panic attacks, anxiety-provoking social situations, traumatic events, or, in the case of specific phobias, exposure to stimuli such as snakes or spiders. At present, there is encouraging evidence for heightened conditionability in anxiety patients relative to healthy control samples (e.g., Grillon & Morgan, 1999;Orr et al., 2000;Pitman & Orr, 1986;Thayer, Friedman, Borkovec, Johnsen, & Molina, 2000), but the implications of these findings for the etiology of anxiety disorders have not been elucidated, and inconsistent findings in the literature have not been adequately addressed.Address correspondence to: Michael W. Otto, Ph.D., Boston University, Center for Anxiety and Related Disorders, 648 Beacon St., 5 th Floor, Boston, MA 02215, Phone: (617) Fax: (617) In these conditioning studies, a stimulus is associated with a mildly-aversive unconditioned stimulus (UCS; e.g., an annoying but not painful shock) during acquisition trials. Autonomic responses, commonly skin conductance response (SCR) or heart rate, are used to measure anticipation of the UCS, and are informally referred to as representing the acquired or "conditioned fear" response to the conditioned stimulus (CS).Conditioned fear responses in humans have been assessed primarily with two different conditioning paradigms. In the first of these procedures, researchers have used the average SCR to a single, repeatedly-presented CS during acquisition as ...
*Wnt signaling regulates -catenin-mediated gene transcription and planar cell polarity (PCP). The Wnt co-receptor, Lrp6, is required for signaling along the -catenin arm. We show that Lrp6 downregulation (by morpholino injection) or overexpression in Xenopus embryos disrupts convergent extension, a hallmark feature of Wnt/PCP components. In embryos with decreased Lrp6 levels, cells of the dorsal marginal zone (DMZ), which undergoes extensive cellular rearrangements during gastrulation, exhibit decreased length:width ratios, decreased migration, and increased numbers of transient cytoplasmic protrusions. We show that Lrp6 opposes Wnt11 activity and localizes to the posterior edge of migrating DMZ cells and that Lrp6 downregulation enhances cortical and nuclear localization of Dsh and phospho-JNK, respectively. Taken together, these data suggest that Lrp6 inhibits Wnt/PCP signaling. Finally, we identify the region of the Lrp6 protein with Wnt/PCP activity to a stretch of 36 amino acids, distinct from regions required for Wnt/-catenin signaling. We propose a model in which Lrp6 plays a critical role in the switch from Wnt/PCP to Wnt/-catenin signaling.
Little is known about cultural differences in the expression of distress in anxiety disorders. Previous cross-cultural studies of depression have found a greater somatic focus in Asian populations. We examined anxiety symptoms in patients with generalized anxiety disorder (GAD) in urban mental health settings in Nepal (N = 30) and in the United States (N = 23). Participants completed the Beck Anxiety Inventory (BAI). The overall BAI score and somatic and psychological subscales were compared. While there was no difference in total BAI scores, the Nepali group scored higher on the somatic subscale (i.e. "dizziness" and "indigestion," t[df] = -2.63[50], p < 0.05), while the American group scored higher on the psychological subscale (i.e. "scared" and "nervous," t[df] = 3.27[50], p < 0.01). Nepali patients with GAD had higher levels of somatic symptoms and lower levels of psychological symptoms than American patients with GAD. Possible explanations include differences in cultural traditions of describing distress and the mind-body dichotomy.
Women have a higher prevalence of generalized anxiety disorder (GAD) than do men, but few studies have assessed gender differences in response to pharmacotherapy. In this study we examined gender as a correlate of response to 6 weeks of open, prospective fluoxetine treatment in 23 men and 22 women with a primary diagnosis of GAD. There was no difference by gender in age or prevalence of mood and anxiety comorbidity; however, GAD onset occurred at a significantly younger age in women compared with men. Despite a lack of difference in baseline severity measures, women had a significantly poorer response to fluoxetine as measured by both the Hamilton Anxiety Rating Scale (HAM-A) and Clinician Global Impression-Severity Scale (CGI-S). In multivariate analyses, there was a significant interaction between age of onset and gender: men with younger age of onset and women with older age of onset exhibited poorer response on the HAM-A. These data, though limited in sample size and by the post hoc nature of our analyses, offer preliminary support that women with GAD, particularly those with a later age of onset, may have a poorer response to the selective serotonin reuptake inhibitor (SSRI) fluoxetine. Larger placebo-controlled trials are needed to more definitively examine gender and treatment response in anxiety disorders.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.