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.
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.
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.
Towards a Model of Travel Fear Fennell, David A.
Annals of tourism research,
September 2017, 2017-09-00, 20170901, Volume:
66
Journal Article
Peer reviewed
•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.
Learning about potential threats is critical for survival. Learned fear responses are acquired either through direct experiences or indirectly through social transmission. Social fear learning (SFL), ...also known as vicarious fear learning, is a paradigm successfully used for studying the transmission of threat information between individuals. Animal and human studies have begun to elucidate the behavioral, neural and molecular mechanisms of SFL. Recent research suggests that social learning mechanisms underlie a wide range of adaptive and maladaptive phenomena, from supporting flexible avoidance in dynamic environments to intergenerational transmission of trauma and anxiety disorders. This review discusses recent advances in SFL studies and their implications for basic, social and clinical sciences.
Observational fear learning in rodents is a type of context-dependent fear conditioning in which an unconditioned stimulus (US) is provided vicariously by observing conspecific others receiving foot ...shocks. This suggests the involvement of affective empathy, with several recent studies showing many similarities between this behavior and human empathy. Neurobiologically, it is important to understand the neural mechanisms by which the vicarious US activates the fear circuit via the affective pain system, obviating the sensory pain pathway and eventually leading to fear memory formation. This paper reviews current studies on the neural mechanisms underlying observational fear learning and provides a perspective on future research on this subject.
Observational fear, a rodent model of affective empathy, is context-dependent fear conditioning in which an unconditioned stimulus is vicariously provided. Keum and Shin discuss neural mechanisms underlying observational fear, highlighting that neural substrates for empathy overlap with observational fear.
Coming to terms with fear LeDoux, Joseph E.
Proceedings of the National Academy of Sciences - PNAS,
02/2014, Volume:
111, Issue:
8
Journal Article
Peer reviewed
Open access
The brain mechanisms of fear have been studied extensively using Pavlovian fear conditioning, a procedure that allows exploration of how the brain learns about and later detects and responds to ...threats. However, mechanisms that detect and respond to threats are not the same as those that give rise to conscious fear. This is an important distinction because symptoms based on conscious and nonconscious processes may be vulnerable to different predisposing factors and may also be treatable with different approaches in people who suffer from uncontrolled fear or anxiety. A conception of so-called fear conditioning in terms of circuits that operate nonconsciously, but that indirectly contribute to conscious fear, is proposed as way forward.
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.