抑制引起的遗忘及其神经机制

当面对不愉快的提醒时, 人们通常会试图阻止那些不想要的记忆出现在脑海中。先前的研究表明, 抑制不想要的记忆的检索会降低这些记忆的可及性, 引起遗忘, 这一效应称为抑制引起的遗忘(suppression- induced forgetting, SIF)。SIF的神经机制涉及右背外侧前额叶皮层和额中回的激活增加, 以及海马的激活受到抑制。SIF的程度受记忆材料的情绪效价、个体的病理性情绪状态和训练的影响。未来研究应在深入了解SIF神经机制的基础上, 考虑如何提高临床病理性记忆的SIF效果, 以达到治疗目的。     

Neural mechanisms of social influence

The present investigation explores the neural mechanisms underlying the impact of social influence on preferences. We socially tagged symbols as valued or not – by exposing participants to the preferences of their peers – and assessed subsequent brain activity during an incidental processing task in which participants viewed popular, unpopular, and novel symbols. The medial prefrontal cortex (mPFC) differentiated between symbols that were and were not socially tagged – a possible index of normative influence – while aspects of the striatum (the caudate) differentiated between popular and unpopular symbols – a possible index of informational influence. These results suggest that integrating activity in these two brain regions may differentiate objects that have become valued as a result of social influence from those valued for non-social reasons.     

人声加工的神经机制

人声是人类听觉环境中最熟知和重要的声音, 传递着大量社会相关信息。与视觉人脸加工类似, 大脑对人声也有着特异性加工。研究者使用电生理、脑成像等手段找到了对人声有特异性反应的脑区, 即颞叶人声加工区(TVA), 并发现非人类动物也有类似的特异性加工区域。人声加工主要涉及言语、情绪和身份信息的加工, 分别对应于三条既相互独立又相互作用的神经通路。研究者提出了双通路模型、多阶段模型和整合模型分别对人声的言语、情绪和身份加工进行解释。未来研究需要进一步讨论人声加工的特异性能否由特定声学特征的选择性加工来解释, 并深入探究特殊人群(如自闭症和精神分裂症患者)的人声加工的神经机制。     

Neural correlates and causal mechanisms

What Joseph Neisser calls for is exactly right: more philosophy of science will help us better understand and refine the idea of neural correlates of consciousness (NCC). But (i) the key bit of philosophy of science Neisser appeals to is itself in need of clarification; (ii) the orthodox NCC definition is more resourceful than Neisser allows, and (iii) it is possible to resist the phenomenological conception of conscious experience that fuels some of Neisser's argument.     

情景记忆成功年老化的神经机制

随着年龄的增长,大部分老年人的情景记忆会出现衰退,但也会有一部分老年人的情景记忆表现出成功的年老化,即记忆成绩较好或随增龄的衰退程度较小。脑保持理论、神经去分化理论、认知储备理论以及神经补偿理论分别从不同角度解释了情景记忆成功年老化的神经机制。基于选择性优化与补偿模型对现有理论进行整合,发现情景记忆成功年老化可能与个体的认知储备水平直接相关：高认知储备的老年人能够对情景记忆相关的脑区和脑网络进行优化且具备更强的神经补偿能力,因而其脑功能(比如,神经表征和神经加工通路的特异性)可能会保持地更好。未来研究需要更多地采用纵向设计来考察各理论之间的关系及其影响因素,从而更好地解释记忆成功年老化的神经机制并为提升老年人的脑与认知健康提供支持。     

Neural mechanisms of affective interference in schizotypy

Negatively valenced stimuli foster cognitive impairment in schizotypy and schizophrenia. To identify relevant brain mechanisms, the authors had 16 positive-schizotypy and 16 control participants perform an emotional Stroop task, judging the ink color of negative and neutral words during functional magnetic resonance imaging (fMRI) of regional brain activity. Schizotypy individuals showed increased right and decreased left activity in dorsolateral prefrontal cortex, indicating a deficit in maintenance of attentional set in the presence of negative emotional distractors. They also showed abnormal activity in ventral limbic areas, including decreased activity in nucleus accumbens and increased activity in hippocampus and amygdala, a circuit involved in the integration of cognitive and affective processes. These results indicate that aspects of emotion-cognition processes and the brain mechanisms that implement them are similar in schizotypy and schizophrenia.     

Contextual control of inhibition with reinforcement: adaptation and timing mechanisms

Four experiments with rats studied the effects of switching the context after Pavlovian conditioning. In three conditioned suppression experiments, a large number of conditioning trials created "inhibition with reinforcement" (IWR), in which fear of the conditional stimulus (CS) reached a maximum and then declined despite continued CS-unconditional stimulus pairings. When IWR occurred, a context switch augmented fear of the CS; IWR and augmentation were highly correlated. Neither IWR nor augmentation resulted from inhibition of delay (IOD): In conditioned suppression, IWR and augmentation occurred without IOD (Experiment 3), and in appetitive conditioning (Experiment 4), IOD occurred without IWR or augmentation. IWR may occur in conditioned suppression because the animal adapts to fear of the CS in a context-specific manner. The authors discuss several implications.     

疼痛恐惧的神经机制及其消退

疼痛恐惧是疼痛基础和临床研究中的一个重要课题。个体对疼痛信息产生过度警觉,诱发不恰当的回避行为,扰乱机体的正常功能,加剧疼痛的现象即为疼痛恐惧。疼痛恐惧可影响个体的疼痛感知以及疼痛相关的注意和回避行为,且在慢性疼痛(如慢性肌骨骼疼痛)的发展、维持个体正常生理功能的丧失中起着重要作用。疼痛恐惧的形成与表达涉及杏仁核、海马、背侧前扣带回皮层、和前额叶皮层等脑区的参与。当前的疼痛恐惧消退的心理-行为干预方法可在疼痛恐惧加工的不同阶段(巩固、再巩固和消退)消退个体的疼痛恐惧。然而,由于恐惧记忆形成过程较为复杂并受多种因素影响,疼痛恐惧记忆消退方法效果较不稳定,其基础研究与临床应用之间仍存在较大的鸿沟。将来研究有必要考虑到疼痛恐惧形成环境的差异以及个体人格特质/心理状态的差异,逐步完善相关消退方法并将其引入临床镇痛,以期帮助患者弱化、擦除甚至改写困扰他们的疼痛恐惧,从而缓解甚至消除病患的疼痛。     

音乐愉悦体验的神经机制

愉悦情绪体验是音乐活动中最普遍的心理现象。通过系统回顾相关的神经科学研究, 认为音乐愉悦体验与大脑奖赏系统的活动有关, 并涉及伏隔核与听觉皮层等其他脑区的交互。在这个过程中, 多巴胺的传递与音乐愉悦体验存在因果联系。基于预期视角, 奖赏预测误差理论和音乐信息理论模型可以解释音乐愉悦体验的产生机制。未来研究应进一步检验伏隔核及各皮层在音乐愉悦体验中的功能, 并整合不同的预期理论。     

Neural and molecular mechanisms of microcognition in Limax

Various non-mammalian model systems are being explored in the search for mechanisms of learning and memory storage of sufficient generality to contribute to the understanding of mammalian learning mechanisms. The terrestrial mollusk Limax maximus is one such model system in which mammalian-quality learning has been documented using odors as conditioned stimuli. The Limax odor information-processing circuits incorporate several system design features also found in mammalian odor-processing circuits, such as the use of cellular and network oscillations for making odor computations and the use of nitric oxide to control network oscillations. Learning and memory formation has been localized to a particular central circuit, the procerebral lobe, in which selective gene activation occurs through odor learning. Since the isolated Limax brain can perform odor learning in vitro, the circuits and synapses causally linked to learning and memory formation are assessable for further detailed analysis.     

双眼视差的神经机制与知觉学习效应

双眼瞳距使得空间某物体在左右眼视网膜的成像存在微小位置差异, 这种差异被称为双眼视差(binocular disparity), 是立体视知觉的重要信息来源。对双眼视差的心理物理学研究始于18世纪初, 迄今已有接近两百年的历史。近年来, 双眼视差研究主要集中在两方面。其一是用电生理、脑成像技术考察双眼视差在视觉背、腹侧通路的模块化表征, 其脑区表征反映出视觉系统的层级式、平行式加工规律。其二是应用知觉学习范式研究双眼视差的可塑性。未来研究应综合脑成像和神经调控技术考察双眼视差的神经机制及其学习效应, 包括双眼视差与多种深度线索间的信息整合和交互作用。应用方向上, 可结合虚拟现实等技术优化训练范式, 实现立体视力的康复和增强。     

Neural mechanisms supporting flexible performance adjustment during development

Feedback processing is crucial for successful performance adjustment following changing task demands. The present event-related fMRI study was aimed at investigating the developmental differences in brain regions associated with different aspects of feedback processing. Children age 8–11, adolescents age 14–15, and adults age 18–24 performed a rule switch task resembling the Wisconsin Card Sorting Task, and analyses focused on different types of negative and positive feedback. All age groups showed more activation in lateral orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), dorsolateral prefrontal cortex (DLPFC), and superior parietal cortex following negative relative to positive performance feedback, but the regions contributed to different aspects of feedback processing and had separable developmental trajectories. OFC was adultlike by age 8–11, whereas parietal cortex was adultlike by age 14–15. DLPFC and ACC, in contrast, were still developing after age 14–15. These findings demonstrate that changes in separable neural systems underlie developmental differences in flexible performance adjustment. Supplementary data from this study are available online at the Psychonomic Society Archive of Norms, Stimuli, and Data, atwww.psychonomic.org/archive.     

风险决策的神经机制:基于啮齿类动物研究

风险决策是在不同选项的结果确定、并且结果出现的概率已知情况下的决策。啮齿类风险决策模型研究发现前额皮层-杏仁核-伏隔核神经环路联系是决定风险决策的选择倾向的关键。前额皮层中的眶额皮层和内侧前额皮层参与风险决策的策略形成和策略转换有关;而皮层下核团中的杏仁核、腹侧纹状体的伏隔核等结构参与策略保持、价值判断,影响决策偏向和行动强度;眶额皮层、伏隔核神经元和多巴胺神经元编码风险决策过程中的概率、风险等因素;此外,多巴胺等单胺类神经递质及受体在风险决策中有复杂的作用。     

Neural dynamics of autistic behaviors: cognitive, emotional, and timing substrates

What brain mechanisms underlie autism, and how do they give rise to autistic behavioral symptoms? This article describes a neural model, called the Imbalanced Spectrally Timed Adaptive Resonance Theory (iSTART) model, that proposes how cognitive, emotional, timing, and motor processes that involve brain regions such as the prefrontal and temporal cortex, amygdala, hippocampus, and cerebellum may interact to create and perpetuate autistic symptoms. These model processes were originally developed to explain data concerning how the brain controls normal behaviors. The iSTART model shows how autistic behavioral symptoms may arise from prescribed breakdowns in these brain processes, notably a combination of underaroused emotional depression in the amygdala and related affective brain regions, learning of hyperspecific recognition categories in the temporal and prefrontal cortices, and breakdowns of adaptively timed attentional and motor circuits in the hippocampal system and cerebellum. The model clarifies how malfunctions in a subset of these mechanisms can, through a systemwide vicious circle of environmentally mediated feedback, cause and maintain problems with them all.     

Neural predictive mechanisms and their role in cognitive incrementalism

Many neuroscientists view prediction as one of the core brain functions, especially on account of its support of fast movements in complex environments. This leads to the natural question whether predictive knowledge forms the cornerstone of our common-sense understanding of the world. However, there is little consensus as to the exact nature of predictive information and processes, or of the neural mechanisms that realize them. This paper compares procedural versus declarative notions of prediction, examines how the brain appears to carry out predictive functions, and discusses to what degree, and at what level, these neural mechanisms support cognitive incrementalism: the notion that high-level cognition stems from sensorimotor behavior.