Current topics in behavioral neurosciences最新文献

Interoception, the process of detecting, perceiving, and interpreting signals from within the body, is essential for physiological regulation and adaptive behavior. A growing body of research underscores important potential links between interoceptive dysfunction and psychiatric disorders. Parallel advancements in the field of computational psychiatry have led to the development of biologically plausible models of information processing in the brain. This review surveys the current state of traditional and computational research approaches to study interoceptive processes in psychiatry. We also provide a foundational description of predominant computational approaches and theoretical models of interoception. Finally, we discuss the potential molecular foundations of interoceptive computation and consider future directions for incorporating computational models to enhance clinical insights and inform personalized treatments. We conclude that combining interoception and computational modeling approaches holds considerable promise in moving the field forward, both in addressing unresolved mechanistic questions and identifying novel potential therapeutic targets.

Behavioral and psychological symptoms of dementia (BPSD), such as agitation, apathy, and psychosis, are highly prevalent and have a significant impact on patients and their care partners. The neurobiology of BPSD involves a complex interplay of structural brain changes and alterations in the neurotransmitter system. Various genetic and plasma biomarkers have also been studied. Research in BPSD has been limited by heterogeneity in the diagnostic criteria and assessment tools. As such, there have been ongoing efforts to develop a gold-standard assessment tool and diagnostic criteria. Current practice guidelines recommend nonpharmacological therapies as first-line treatments. Pharmacological options are often used when there is an insufficient response to nonpharmacological strategies, but there can be serious adverse effects with existing pharmacological agents. This has resulted in growing efforts to develop novel therapeutics with more favorable tolerability profiles, with some showing promising results. Other biological therapies, such as neurostimulation, have also demonstrated positive results. As our understanding of BPSD evolves, ongoing research efforts in treatment of BPSD are warranted in order to enhance the quality of life for patients and their care partners.

Anxiety disorders in children lead to substantial impairment in functioning and development. Even the most effective gold standard treatments for childhood anxiety have 50% remission rates, suggesting a critical need to improve current treatments. Optimising exposure, the key component of anxiety treatments, represents a promising way to do so. This chapter explains how to optimise exposure outcomes for childhood anxiety through inhibitory learning theory. This chapter describes the background of inhibitory learning, including its different components and the empirical evidence supporting it. We then discuss how to improve the formation of inhibitory associations through enhancing expectancy violation, the proposed mechanism underlying inhibitory learning. Strategies to enhance inhibitory learning for child anxiety treatment are provided. These include strategies to enhance the formation of inhibitory associations, such as psychoeducation, eliminating safety signals, deepened extinction, occasional reinforced extinction, and affect-based strategies. Additionally, strategies to enhance retrieval include variability, multiple contexts, and retrieval cues. Suggestions are made on how to adapt these strategies to child populations. Further, a clinical guide for using inhibitory learning strategies in child anxiety treatment is included as an appendix. This details how clinicians can utilise these strategies to enhance current treatments, including examples of case studies and scripts.

In the last two decades, the endocannabinoid system has emerged as a crucial modulator of motivation and emotional processing. Due to its widespread neuroanatomical distribution and characteristic retrograde signaling nature, cannabinoid type I receptors and their endogenous ligands finely orchestrate somatic and axon terminal activity of dopamine neurons. Owing to these unique features, this signaling system is a promising pharmacological target to ameliorate dopamine-mediated drug-seeking behaviors while circumventing the adverse side effects of, for instance, dopaminergic antagonists. Despite considerable preclinical efforts, an agreement on the efficacy of endocannabinoid-targeting compounds for treating drug substance use disorders in humans has not been reached. In the following chapter, we will summarize preclinical and clinical evidence addressing the therapeutic potential of cannabinoids and endocannabinoid-targeting compounds in substance use disorders. To bridge the gap between animal and clinical research, we capitalize on studies evaluating the impact of endocannabinoid-targeting compounds in relevant settings, such as the management of drug relapse. Finally, we discuss the therapeutic potential of novel cannabinoid compounds that hold promise for treating substance use disorders.

This chapter explores the risks of guruism and cultic social dynamics in organisations that work with psychedelic drugs, which include therapist offices, clinics, research departments, retreat centres, training programmes, NGOs, underground ceremonies and new religious movements. It has been hypothesised, and argued by experienced practitioners, that psychedelics can increase suggestibility, amplify transference and facilitate an intense form of projective mechanisms in the recipients. They may thereby lead to ego-inflation and feelings of grandiosity and omnipotence in those giving the drugs and intensify cultic social dynamics in psychedelic communities - all of which can create conditions that make cases of harm and misconduct more likely to occur and go unreported. This chapter briefly introduces the terms 'guruism' and 'cultic social dynamics' and how these dynamics can lead to harm and abuse and then discusses how psychedelic drugs might amplify these processes, before outlining possible safeguards.

A decline in hippocampal function has long been associated with the progression of cognitive impairments in patients with Alzheimer's disease (AD). The disruption of hippocampal synaptic plasticity [primarily the reduction of long-term potentiation LTP] by excess production of soluble beta-amyloid (Aβ) has long been accepted as the mechanism by which AD pathology impairs memory, at least during the early stages of AD pathogenesis. However, the premise that hippocampal LTP underpins the formation of associative, long-term memories has been challenged. Here, we consider evidence that this canonical view of LTP needs to be refined. Similarly, the view that the hippocampus simply supports memory ignores the wealth of data showing that the hippocampus is functionally heterogeneous along its septo-temporal axis. The ventral (but not the dorsal) hippocampus plays a major role in modulating emotional reactions to conflict. Here, we suggest that hippocampal LTP is not involved in forming long-term associative memories, but instead contributes to the disambiguation of overlapping memories in situations of conflict and associative interference. This conceptualisation of hippocampal synaptic plasticity may help explain how early-stage AD pathology may impact both memory and anxiety.

The elucidation of the functional neuroanatomy of human fear, or threat, extinction has started in the 2000s by a series of enthusiastically greeted functional magnetic resonance imaging (fMRI) studies that were able to translate findings from rodent research about an involvement of the ventromedial prefrontal cortex (vmPFC) and the hippocampus in fear extinction into human models. Enthusiasm has been painfully dampened by a meta-analysis of human fMRI studies by Fullana and colleagues in 2018 who showed that activation in these areas is inconsistent, sending shock waves through the extinction research community. The present review guides readers from the field (as well as non-specialist readers desiring safe knowledge about human extinction mechanisms) during a series of exposures with corrective information. New information about extinction-related brain activation not considered by Fullana et al. will also be presented. After completion of this exposure-based fear reduction program, readers will trust that the reward learning system, the cerebellum, the vmPFC, the hippocampus, and a wider brain network are involved in human fear extinction, along with the neurotransmitters dopamine and noradrenaline. Specific elements of our exposure program include exploitation of the temporal dynamics of extinction, of the spatial heterogeneity of extinction-related brain activation, of functional connectivity methods, and of large sample sizes. Implications of insights from studies in healthy humans for the understanding and treatment of anxiety-related disorders are discussed.

Research on emotion regulation often focuses on cognitively effortful self-regulation strategies, but exposure to stress has been shown to interfere with the underlying mechanisms supporting such processes. Understanding alternative strategies that potentially bolster emotion regulation under stress is an important topic of investigation. Two potential alternatives involve everyday occurrences of social processing and memory recall. Social support and past emotional experiences may help in guiding us toward appropriate neurophysiological responses through overlapping circuitry with stress and reward systems, while also buttressing cognitive regulation strategies by expanding one's perspective and allowing multiple opportunities to regulate retrospectively. In recognition that ongoing social and emotional events are often at the beginning of a cascade of both emotion regulation and memory processes, this chapter focuses on the emerging role of social relationships and autobiographical memory recall in regulating emotions under stress, highlighting opportunities and challenges associated with this process.