The Neuropsychological Bases of Category Learning

There is a long history of research into how people learn new categories of objects or events. Recent advances have led to new insights about the neuropsychological basis of this critically important cognitive process. In particular, there is now good evidence that the frontal cortex and basal ganglia contribute to category learning, that medial temporal lobe structures make a more minor contribution, and that categorization rules are not represented in visual cortex. There is also strong evidence that normal category learning is mediated by at least two separate systems. A recent neuropsychological theory of category learning that is consistent with these data is described.     

Involvement of amygdala in inhibitory control over aggression in the rat: A synopsis

An experimentally produced hyperreactivity facilitates initiation of mouse-killing in rats that did not previously develop any stable inhibition of interspecific aggression. Destruction of the corticomedial amygdala or interruption of the stria terminalis interferes with the development of such an inhibition on the basis of “social” influences, whereas lateral amygdaloid lesions have no effect on mouse-killing.     

Shock-induced aggression and pain sensitivity in the rat: Catecholamine involvement in the corticomedial amygdala

The possible role of amygdaloid catecholamines in the control of shock-induced aggression and pain sensitivity in the rat was investigated. Bilateral microinjections of chlorpromazine into the corticomedial amygdala resulted in decreased fighting and decreased sensitivity to the shock stimulus. Further analysis of this effect, using specific adrenergic antagonists, revealed that neither a- nor Padrenergic systems appeared to be responsible for the behavioral effect of chlorpromazine. Injections of haloperidol into the same region, however, yielded a reduction similar to that produced by chlorpromazine, while dopamine injections resulted in significant elevations in both fighting and pain sensitivity. No effect on any of these behavioral measures was obtained following injection of any of the agents into the basolateral amygdala. These results suggest that the observed effect of catecholamine injections in the corticomedial amygdala is related to changes in pain sensitivity mediated by dopamine.     

右侧基底节损伤遗忘症患者的知觉性启动效应与语义性启动效应的分离与定位

采用偏好、自由联想、字根补笔和字辨认等4项任务观察一例单纯性右侧基底节损伤遗忘症患者和两组正常对照的启动效应。结果发现：（1）该患者知觉性启动效应障碍,而语义性启动效应正常。认为知觉性启动效应的神经学基础可能在基底节。（2）该患者知觉性启动效应与语义性启动效应分离。认为神经组织的损伤可导致不同形式启动效应的分离,提出内隐记忆或启动效应的不同形式可能存在不同的神经学基础。     

神经质人格的神经生理基础

神经质作为一种人格特质, 核心特征是具有负性情绪体验的倾向。高神经质个体表现出更强的情绪反应、更差的情绪感知和应对, 因而体验到更多的负性情绪, 进而容易形成一系列精神障碍和身体疾病。因此, 神经质成为精神病理学中一个重要的风险因素。来自自主神经系统、神经内分泌系统和脑的证据发现, 高神经质个体心血管灵活性降低、HPA轴基线活动增强、EEG活动增大以及负性情绪引起的杏仁核活动增强, 其中杏仁核的自上而下和自下而上通路可能是整合多方面证据的关键。进一步研究应致力于将遗传学、电生理学、生物化学、脑成像技术等相结合, 构建神经质产生、形成的神经生理模型。     

分类和概念对恐惧泛化的影响机制

恐惧泛化与多种焦虑障碍的病理基础密切相关。例如创伤后应激障碍个体往往持续地逃避与创伤事件有关的刺激,遭受着创伤痛苦折磨。本文在厘清知觉辨别与恐惧泛化关系的基础上,着力于高级认知过程(分类与概念相似性、典型性和人工概念)对恐惧泛化的影响,回顾了恐惧泛化的相关神经机制,并揭示恐惧泛化对焦虑障碍患者的临床治疗启示。未来研究应将知觉和高级认知维度的恐惧泛化进行整合研究,同时扩充恐惧习得和泛化的神经回路,以促进人类恐惧泛化更深入的研究。     

人类情绪记忆的行为遗传学与神经遗传学研究进展述评

情绪记忆及其增强效应存在广泛的个体差异,这种个体差异可能有其神经与遗传基础。近来的行为遗传学与神经遗传学证实人类ADRA2B基因缺失突变以及BDNF Val66Met基因的多态性与情绪记忆增强及其神经机制的个体差异相联系。本文重点介绍与人类情绪记忆相关的这两种基因,梳理了行为与神经遗传学研究的最新进展,指出未来应关注更多候选基因,并重视多个脑区之间的交互作用;还应使用情绪面孔刺激探索BDNF Val66Met基因多态性对情绪记忆编码和提取的影响等。     

厌恶加工的神经基础

厌恶是由令人不愉悦、反感的事物诱发的情绪。根据刺激类型的不同, 厌恶可以分为不同的类型。脑岛和基底节是厌恶加工的主要脑区, 前扣带回、杏仁核、丘脑、内侧前额叶也参与厌恶加工。对已有研究的总结发现, 不同类型的厌恶、不同感觉通道的厌恶加工可能具有不同的神经基础。在未来的研究中, 应当注重研究厌恶加工的认知机制、神经基础以及与厌恶相关的神经递质等问题。     

The effects of lesions in the central nucleus of the amygdala on appetitive classical conditioning in rats

Abstract: Lesions in the central nucleus of the amygdala (cAMY) have been known to interfere with the acquisition of fear classical conditioning when footshock is used as an unconditioned stimulus (US). The present study examined whether or not a similar interference would occur with an appetitive US. Five rats with lesions in the cAMY (the cAMY group), and eight unoperated control rats were trained in an appetitive classical conditioning paradigm, which did not include elements of operant learning, using a visual conditioned stimulus (CS) (5 W of light for 10 s duration) paired with a food pellet US (45 mg, cheese flavor). The behavioral index of appetitive conditioning was an increase in rearing approach behavior to the CS after CS and US pairings. During CS and US pairings, the movement of the rat was limited so that this approach behavior could not occur. As a result, all control rats showed an increase in rearing, but the cAMY group did not. These results suggest that the cAMY is critical for appetitive as well as fear classical conditioning.     

Structural and Functional Neuroplasticity in Relation to Traumatic Stress

ABSTRACT— The body's stress response is an essential adaptive and protective mechanism to cope with threatening situations. However, chronic or traumatic stress leads to structural and functional alterations in the traumatized brain. We argue for a building-block effect: Exposure to different types of traumatic events increases the probability of developing posttraumatic stress disorder (PTSD), via incremental enlargement of a fear network. We summarize evidence of brain changes in PTSD, including recent results from research on animal models of stress-related neuroplastic remodeling, with an emphasis on structural and functional changes in the hippocampus, the amygdala, and the medial prefrontal cortex.