Current topics in behavioral neurosciences最新文献

Currently available therapeutic modalities for alcohol use disorder (AUD) produce limited effect sizes or long-term compliance. Recent methods that were developed to modulate brain activity represent potential novel treatment options. Various methods of brain stimulation, when applied repeatedly, can induce long-term neurobiological, behavioral, and cognitive modifications. Recent studies in alcoholic subjects indicate the potential of brain stimulation methods to reduce alcohol craving, consumption, and relapse. Specifically, deep brain stimulation (DBS) of the nucleus accumbens or non-surgical stimulation of the dorsolateral prefrontal cortex (PFC) or medial PFC and anterior cingulate cortex using transcranial magnetic stimulation (TMS) has shown clinical benefit. However, further preclinical and clinical research is needed to establish understanding of mechanisms and the treatment protocols of brain stimulation for AUD. While efforts to design comparable apparatus in rodents continue, preclinical studies can be used to examine targets for DBS protocols, or to administer temporal patterns of pulsus similar to those used for TMS, to more superficial targets through implanted electrodes. The clinical field will benefit from studies with larger sample sizes, higher numbers of stimulation sessions, maintenance sessions, and long follow-up periods. The effect of symptoms provocation before and during stimulation should be further studied. Larger studies may have the power to explore predictive factors for the clinical outcome and thereby to optimize patient selection and eventually even develop personalization of the stimulation parameters.

The use of animal models continues to be essential for carrying out research into clinical phenomena, including addiction. However, the complexity of the clinical condition inevitably means that even the best animal models are inadequate, and this may go some way to account for the apparent failures of discoveries from animal models, including the identification of potential novel therapies, to translate to the clinic. We argue here that it is overambitious and misguided in the first place to attempt to model complex, multifacetted human disorders such as addiction in animals, and especially in rodents, and that all too frequently "validity" of such models is limited to superficial similarities, referred to as "face validity", that reflect quite different underlying phenomena and biological processes from the clinical situation. Instead, a more profitable approach is to identify (a) well-defined intermediate human behavioural phenotypes that reflect defined, limited aspects of, or contributors to, the human clinical disorder, and (b) to develop animal models that are homologous with those discrete human behavioural phenotypes in terms of psychological processes, and underlying neurobiological mechanisms. Examples of past and continuing weaknesses and suggestions for more limited approaches that may allow better homology between the test animal and human condition are made.

The gut microbiota is constituted by trillions of microorganisms colonizing the human intestine. Studies conducted in patients with alcohol use disorder (AUD) have shown altered microbial composition related to bacteria, viruses, and fungi.This review describes the communication pathways between the gut and the brain, including the ones related to the bacterial metabolites, the inflammatory cytokines, and the vagus nerve. We described in more detail the gut-derived metabolites that have been shown to be implicated in AUD or that could potentially be involved in the development of AUD due to their immune and/or neuroactive properties, including tryptophan-derivatives, tyrosine-derivatives, short chain fatty acids.Finally, we discussed the potential beneficial effects of microbiome-based therapies for AUD such as probiotics, prebiotics, postbiotic, and phage therapy.

Alcohol impacts neural circuitry throughout the brain and has wide-ranging effects on the biophysical properties of neurons in these circuits. Articulating how these wide-ranging effects might eventually result in altered computational properties has the potential to provide a tractable working model of how alcohol alters neural encoding. This chapter reviews what is currently known about how acute alcohol influences neural activity in cortical, hippocampal, and dopaminergic circuits as these have been the primary focus of understanding how alcohol alters neural computation. While other neural systems have been the focus of exhaustive work on this topic, these brain regions are the ones where in vivo neural recordings are available, thus optimally suited to make the link between changes in neural activity and behavior. Rodent models have been key in developing an understanding of how alcohol impacts the function of these circuits, and this chapter therefore focuses on work from mice and rats. While progress has been made, it is critical to understand the challenges and caveats associated with experimental procedures, especially when performed in vivo, which are designed to answer this question and if/how to translate these data to humans. The hypothesis is discussed that alcohol impairs the ability of neural circuits to acquire states of neural activity that are transiently elevated and characterized by increased complexity. It is hypothesized that these changes are distinct from the traditional view of alcohol being a depressant of neural activity in the forebrain.

Dissociative symptoms and disorders of dissociation are characterised by disturbances in the experience of the self and the surrounding world, manifesting as a breakdown in the normal integration of consciousness, memory, identity, emotion, and perception. This paper aims to provide insights into dissociative symptoms from the perspective of interoception, the sense of the body's internal physiological state, adopting a transdiagnostic framework.Dissociative symptoms are associated with a blunting of autonomic reactivity and a reduction in interoceptive precision. In addition to the central function of interoception in homeostasis, afferent visceral signals and their neural and mental representation have been shown to shape emotional feeling states, support memory encoding, and contribute to self-representation. Changes in interoceptive processing and disrupted integration of interoceptive signals into wider cognition may contribute to detachment from the body and the world, blunted emotional experience, and altered subjective recall, as experienced by individuals who suffer from dissociation.A better understanding of the role of altered interoceptive integration across the symptom areas of dissociation could thus provide insights into the neurophysiological mechanisms underlying dissociative disorders. As new therapeutic approaches targeting interoceptive processing emerge, recognising the significance of interoceptive mechanisms in dissociation holds potential implications for future treatment targets.

The contemporary neuroscience understanding of the brain as an active inference organ supports that our conscious experiences, including sensorimotor perceptions, depend on the integration of probabilistic predictions with incoming sensory input across hierarchically organized levels. As in other systems, these complex processes are prone to error under certain circumstances, which may lead to alterations in their outcomes (i.e., variations in sensations and movements). Such variations are an important aspect of functional neurological disorder, a complex disorder at the interface of brain-mind-body interactions. Thus, predictive processing frameworks offer fundamental mechanistic insights into the pathophysiology of functional neurological disorder. In recent years, many of the aspects relevant to the neurobiology of functional neurological disorder - e.g., aberrant motor and sensory processes, symptom expectation, self-agency, and illness beliefs, as well as interoception, allostasis, and emotion - have been investigated through the lens of predictive processing frameworks. Here, we provide an overview of the current state of research on predictive processing and the pathophysiology of functional neurological disorder.

Eating disorders (EDs) are characterized by abnormal responses to food and weight-related stimuli and are associated with significant distress, impairment, and poor outcomes. Because many of the cardinal symptoms of EDs involve disturbances in perception of one's body or abnormal affective or cognitive reactions to food intake and how that affects one's size, there has been longstanding interest in characterizing alterations in sensory perception among differing ED diagnostic groups. Within the current review, we aimed to critically assess the existing research on exteroceptive and interoceptive perception and how sensory perception may influence ED behavior. Overall, existing research is most consistent regarding alterations in taste, visual, tactile, and gastric-specific interoceptive processing in EDs, with emerging work indicating elevated respiratory and cardiovascular sensitivity. However, this work is far from conclusive, with most studies unable to speak to the precise etiology of observed perceptual differences in these domains and disentangle these effects from affective and cognitive processes observed within EDs. Further, existing knowledge regarding perceptual disturbances in EDs is limited by heterogeneity in methodology, lack of multimodal assessment protocols, and inconsistent attention to different ED diagnoses. We propose several new avenues for improving neurobiology-informed research on sensory processing to generate actionable knowledge that can inform the development of innovative interventions for these serious disorders.

Phenomenological observations of individuals with body dysmorphic disorder (BDD), coupled with evidence from neuropsychological, psychophysical, and neuroimaging studies, support a model of aberrant visual perception characterized by deficient global/holistic, enhanced detail/local processing, and selective visual-attentional biases. These features may contribute to the core symptomatology of distorted perception of their appearance, in addition to misinterpretation of others' facial expressions and poor insight regarding their misperceived appearance defects. Insights from visual processing studies can contribute to the development of novel interventions, such as perceptual retraining and non-invasive neuromodulation. However, much remains to be understood about visual perception in BDD. Future research should leverage brain imaging modalities with high temporal resolutions and employ study designs that induce conflicts in multisensory integration, thereby advancing our mechanistic understanding of distorted visual perception observed in BDD.

In the aftermath of psychological trauma, many individuals experience perturbations in interoception, a term that broadly references the ability to accurately detect body signals and integrate these signals with emotional states. These interoceptive disruptions can manifest in different ways, including blunting or amplification of sensitivity to internal physiological signals. In this chapter we review extant neurophysiological research on interoception in trauma-exposed populations, with a particular focus on the effects of chronic interpersonal trauma, such as childhood maltreatment and racial discrimination. We explore research that used different types of interoceptive assays, from self-report measures to electrophysiological and neuroimaging tools to characterize the disruptions in pain perception, interoceptive acuity, and physiological responses that may arise after a traumatic event. Finally, we discuss interventions that are designed to target interoceptive mechanisms, from exposure-based therapies to mindfulness-based practices, as well as future directions in trauma interoception research.