Over the past decades, behaviour and cognitive psychology have produced fruitful and mutually converging theories from which hypotheses could be derived on the nature and origin of fear and anxiety ...disorders. Notwithstanding the emergence of effective treatments, there are still many questions that remain to be answered. Here, I will argue that the burgeoning field of behavioural neuroscience may advance our understanding of fear, anxiety disorders and its treatments. Decades of fear-conditioning research across species have begun to elucidate the neurobiological mechanisms underlying associative fear learning and memory. The fear-conditioning paradigm provides a well-controlled and fine-grained research platform to examine these processes. Although the traditional fear conditioning paradigm was originally designed to unveil general principles of fear (un)learning, it is well-suited to understand the transition from normal fear to pathological fear and the mechanisms of change. This paper presents 1) a selection of fear conditioning studies on the generalization and persistence of associative fear memory as intermediate phenotypes of fear and anxiety disorders, and 2) insights from neuroscience on the malleability of fear memory with the potential to provide a long-term cure for anxiety and related disorders.
•Behavioural neuroscience advances our understanding of fear and anxiety disorders.•Fear and anxiety disorders are characterized by associative fear memory.•Fear conditioning is an excellent platform to examine associative fear memory.•Generalization and persistence of fear explain the transition to anxiety disorders.•Insights into the mechanisms of change are crucial to advance treatments.
Learning and memory for extinction of conditioned fear is a basic mammalian mechanism for regulating negative emotion. Sleep promotes both the consolidation of memory and the regulation of emotion. ...Sleep can influence consolidation and modification of memories associated with both fear and its extinction. After brief overviews of the behavior and neural circuitry associated with fear conditioning, extinction learning, and extinction memory in the rodent and human, interactions of sleep with these processes will be examined. Animal and human studies suggest that sleep can serve to consolidate both fear and extinction memory. In humans, sleep also promotes generalization of extinction memory. Time-of-day effects on extinction learning and generalization are also seen. Rapid eye movement (REM) may be a sleep stage of particular importance for the consolidation of both fear and extinction memory as evidenced by selective REM deprivation experiments. REM sleep is accompanied by selective activation of the same limbic structures implicated in the learning and memory of fear and extinction. Preliminary evidence also suggests extinction learning can take place during slow wave sleep. Study of low-level processes such as conditioning, extinction, and habituation may allow sleep effects on emotional memory to be identified and inform study of sleep's effects on more complex, emotionally salient declarative memories. Anxiety disorders are marked by impairments of both sleep and extinction memory. Improving sleep quality may ameliorate anxiety disorders by strengthening naturally acquired extinction. Strategically timed sleep may be used to enhance treatment of anxiety by strengthening therapeutic extinction learned via exposure therapy.
COVID-19 is a major source of fear, stress, and anxiety as well as a major factor impacting the health and wellbeing of people worldwide. The present study builds on the recently developed “Fear of ...COVID-19 Scale” (Ahorsu et al., In International Journal of Mental Health and Addiction,
https://doi.org/10.1007/s11469-020-00270-8
, 2020). The sample comprised of 850 participants, male and female young adults from Russia and Belarus. The majority of survey participants are university students and graduates. Females, students, and others from Russia report higher levels of COVID-19-related fear than those from Belarus. Respondents from Russia and Belarus report less fear than people from Iran who were surveyed earlier. The scale used for the present survey evidenced a good Cronbach’s Alpha measure of internal consistency or reliability (0.809). Clearly, further research is needed across locations and over time about the nature and extent of fear caused by COVID 19. Overall, the FCV-19S appears to be a valuable and brief instrument that may provide useful information for intervention and policy purposes to migrate fear and problem behavior linked to infectious disease outbreaks.
The nonapeptide, oxytocin (OT), known for its role in social bonding and attachment formation, has demonstrated anxiolytic properties in animal models and human studies. However, its role in the ...regulation of fear responses appears more complex, brain site-specific, sex-specific, and dependent on a prior stress history. Studies have shown that OT neurons in the hypothalamus are activated during cued and contextual fear conditioning and during fear recall, highlighting the recruitment of endogenous oxytocin system in fear learning. OT is released into the extended amygdala, which contains the central nucleus of the amygdala (CeA) and the bed nucleus of the stria terminalis (BNST), both critical for the regulation of fear and anxiety-like behaviors. Behavioral studies report that OT in the CeA reduces contextual fear responses; whereas in the BNST, OT receptor (OTR) neurotransmission facilitates cued fear and reduces fear responses to un-signaled, diffuse threats. These ostensibly contrasting behavioral effects support growing evidence that OT works to promote fear discrimination by reducing contextual fear or fear of diffuse threats, yet strengthening fear responses to imminent and predictable threats. Recent studies from the basolateral nucleus of the amygdala (BLA) support this notion and show that activation of OTR in the BLA facilitates fear discrimination by increasing fear responses to discrete cues. Also, OTR transmission in the CeA has been shown to mediate a switch from passive freezing to active escape behaviors in confrontation with an imminent, yet escapable threat but reduce reactivity to distant threats. Therefore, OT appears to increase the salience of relevant threat-signaling cues yet reduce fear responses to un-signaled, distant, or diffuse threats. Lastly, OTR signaling has been shown to underlie emotional discrimination between conspecifics during time of distress, social transmission of fear, and social buffering of fear. As OT has been shown to enhance salience of both positive and negative social experiences, it can also serve as a warning system against potential threats in social networks. Here, we extend the social salience hypothesis by proposing that OT enhances the salience of relevant environmental cues also in non-social contexts, and as such promotes active defensive behaviors.
Towards a Model of Travel Fear Fennell, David A.
Annals of tourism research,
September 2017, 2017-09-00, 20170901, Letnik:
66
Journal Article
Recenzirano
•Fear in tourism is a constellation of different intensities and kinds.•The Model of Travel Fear has six stages.•The model is built not only from tourism research, but also from science outside the ...tourism domain.•Future studies should focus on testing the model empirically.•The model has practical utility.
The aim of this paper was to identify and better understand factors and conditions related to fear in travel. A review of literature on concepts such as constraints, shock, panic, risk, anxiety, and worry provided the necessary content from which to both summarize the tourism literature on fear, and also formulate a Model of Travel Fear. This model, developed through content analysis of the literature, and student trip summaries, is comprised of six main components. These include Characteristics of the tourist, Fear-inducing factors of a trip, Strategies to reduce (or amplify) fear, Travel stage, Fear intensity, and Fear responses. Suggestions were made for future research, particularly empirical testing of the model, and for applications of the model in the tourism industry.
The measurement of Pavlovian forms of fear extinction offers a relatively simple behavioral preparation that is nonetheless tractable, from a translational perspective, as an approach to study ...mechanisms of exposure therapy and biological underpinnings of anxiety and trauma-related disorders such as post-traumatic stress disorder (PTSD). Deficient fear extinction is considered a robust clinical endophenotype for these disorders and, as such, has particular significance in the current “age of RDoC (research domain criteria).” Various rodent models of impaired extinction have thus been generated with the objective of approximating this clinical, relapse prone aberrant extinction learning. These models have helped to reveal neurobiological correlates of extinction circuitry failure, gene variants, and other mechanisms underlying deficient fear extinction. In addition, they are increasingly serving as tools to investigate ways to therapeutically overcome poor extinction to support long-term retention of extinction memory and thus protection against various forms of fear relapse; modeled in the laboratory by measuring spontaneous recovery, reinstatement and renewal of fear. In the current article, we review models of impaired extinction built around (1) experimentally induced brain region and neural circuit disruptions (2) spontaneously-arising and laboratory-induced genetic modifications, or (3) exposure to environmental insults, including stress, drugs of abuse, and unhealthy diet. Collectively, these models have been instrumental in advancing in our understanding of extinction failure and underlying susceptibilities at the neural, genetic, molecular, and neurochemical levels; generating renewed interest in developing novel, targeted and effective therapeutic treatments for anxiety and trauma-related disorders.
It is well known that long-term consolidation of newly acquired information, including information related to social fear, require de novo protein synthesis. However, the temporal dynamics of protein ...synthesis during the consolidation of social fear memories is unclear. To address this question, mice received a single systemic injection with the protein synthesis inhibitor, anisomycin, at different time-points before or after social fear conditioning (SFC), and memory was assessed 24 h later. We showed that anisomycin impaired the consolidation of social fear memories in a time-point-dependent manner. Mice that received anisomycin 20 min before, immediately after, 6 h, or 8 h after SFC showed reduced expression of social fear, indicating impaired social fear memory, whereas anisomycin caused no effects when administered 4 h after SFC. These results suggest that consolidation of social fear memories requires two stages of protein synthesis: (1) an initial stage starting during or immediately after SFC, and (2) a second stage starting around 6 h after SFC and lasting for at least 5 h.
OBJECTIVES
To determine the prevalence of fear of falling (FOF) and fear‐related activity restriction (FAR) and their association with frailty, sarcopenia, gait speed and grip strength, cognitive ...impairment, depression, social isolation, self‐perceived health, and vision.
DESIGN
Observational cross‐sectional study.
SETTING
Community.
PARTICIPANTS
A total of 493 community‐dwelling older adults, 60 years and older.
MEASURES
FOF and FAR were assessed using validated single closed‐ended questions. Questionnaire was administered to evaluate frailty (FRAIL scale ‐ Fatigue, Resistance, Aerobic, Illness, and Loss of Weight), sarcopenia (SARC‐F ‐ lifting and carrying 10 pounds, walking across a room, transferring from bed/chair, climbing a flight of 10 stairs, and frequency of falls in the past 1 year), social isolation (six‐item Lubben Social Network Scale), depression (Even Briefer Assessment Scale), cognition (Chinese Mini‐Mental State Examination), and perceived general health and pain (The EuroQol‐5 Dimension (EQ‐5D)and EQ visual analogue scale (EQ VAS)) . Binary logistic regression was performed to determine the influence of sociodemographic, medical, functional, and cognitive variables on FOF with/without FAR.
RESULTS
Prevalence of FOF was 69.2%, and among them, 38.4% had FAR. Prevalence of FOF with or without FAR in those with sarcopenia was 93.3% and in prefrail/frail was 76.6%. FOF was significantly associated with prefrail/frail (odds ratio (OR) = 2.17; 95% confidence interval (CI) = 1.26–3.73), depression (OR = 4.90; 95% CI = 1.06–22.67), number of medications (OR = 1.28; 95% CI = 1.03–1.59), and female sex (OR = 3.54; 95% CI = 1.82–6.90). FOF + FAR was associated with depression (OR = 5.17; 95% CI = 1.84–14.54) and sarcopenia (OR = 8.13; 95% CI = 1.52–43.41).
CONCLUSION
FOF with/without FAR is highly prevalent among community‐dwelling older adults, especially in those with sarcopenia, prefrailty, and frailty, with significant negative impact on function, quality of life, social network, and mental health. Further research is needed to investigate the value of population‐level screening, causal relationship, and efficacy of comprehensive intervention strategies.
Post-traumatic stress disorder (PTSD) is a psychiatric disorder associated with memories of traumatic experiences. Conditioned fear memory, a representative model of traumatic memories, is observed ...across species from lower to higher animals, including humans. Numerous studies have investigated the mechanisms of conditioned fear memory and have led to the identification of the underlying processes involved in fear memory regulation, including cellular and systems consolidation of fear conditioning, destabilization/reconsolidation and extinction after fear memory retrieval, and forgetting of fear memory. These studies suggested that mechanisms for fear memory regulation are shared by humans and other higher animals. Additionally, rodent studies have identified the mechanisms of fear memory at the molecular, cellular, and circuit levels. Findings from these studies in rodents have been applied to facilitate the development and improvement of PTSD intervention. For instance, reconsolidation and extinction of fear memories have been applied for PTSD treatment to improve prolonged exposure (PE) therapy, an effective psychotherapy for PTSD. Combination of medications weakening retrieved traumatic memory (e.g., by facilitating both destabilization and extinction) with PE therapy may contribute to improvement of PTSD. Interestingly, a recent study in mice identified forgetting of fear memory as another potential therapeutic target for PTSD. A better understanding of the mechanisms involved in fear memory processes is likely to facilitate the development of better treatments for PTSD. This review describes fear memory processes and their mechanisms and discusses the pros and cons of applying how this knowledge can be applied in the development of interventions for PTSD.
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