非人灵长类的抑制控制能力

抑制控制能力是指个体为实现特定目标对干扰性优势反应进行抑制的能力,是一种高级认知能力。该文综述了对非人灵长类抑制控制能力的研究,从抑制控制能力的行为表现,生理机制及其发生、发展几个方面进行了阐述,提供了一个从演化的角度理解人类的抑制控制能力的视角。     

Understanding Cognition Through Large-Scale Cortical Networks

An emerging body of evidence from a number of fields is beginning to reveal general neural principles underlying cognition. The characteristic adaptability of cognitive function is seen to derive from large-scale networks in the cerebral cortex that are able to repeatedly change the state of coordination among their constituent areas on a subsecond time scale. Experimental and theoretical studies suggest that large-scale network dynamics operate in a metastable regime in which the interdependence of cortical areas is balanced between integrating and segregating activities. Cortical areas, through their coordination dynamics, are thought to rapidly resolve a large number of mutually imposed constraints, leading to consistent local states and a globally coherent state of cognition.     

关联记忆的神经机制研究述评

关联记忆与来源记忆存在很多相似之处,但也存在一定的差异。与项目记忆相比,关联记忆需要参与的大脑区域相对较多,包括前额区与海马等;电生理研究、成像研究以及病人研究都为这一观点提供了可靠的证据。     

氟哌啶醇干扰决策过程中前扣带回神经元的放电活动

运用在体多通道神经元放电同步记录技术, 观察和记录大鼠在完成T-迷宫成本效益决策任务时前扣带回神经元放电和局部场电位的变化及氟哌啶醇对此的改变, 在细胞水平上探讨前扣带回在决策中的作用以及多巴胺递质系统对决策的作用机制。结果显示, 经过一段时间的训练, 10只大鼠中有8只偏好高付出-高奖赏端, 且在选择高付出-高奖赏端时的神经元放电频率要显著高于选择低付出-低奖赏端时的频率, 同时局部场电位也呈现出事件相关性; 腹腔注射多巴胺受体拮抗剂氟哌啶醇后, 大鼠不再偏好高付出-高奖赏端, 对该端的选择显著减少, 而对低付出-低奖赏端的选择显著增加, 且神经元的放电频率和局部场电位显著降低, 神经元放电和局部场电位的特征性也消失。研究提示, 前扣带回和多巴胺在努力相关决策任务中有着至关重要的作用。     

特殊的视错觉：运动诱导视盲

突显的静止目标被一定空间范围内运动背景所覆盖时, 人类会感受到静止目标消失再重现的发生, 这种视错觉现象叫做运动诱导视盲(motion-induced blindness, MIB)。该现象成因的理论解释主要有：注意竞争理论、知觉完型加工理论以及神经生理机制相关理论。作为特殊的视错觉现象, 该现象与其他盲视现象不同,主要是由客体识别过程中的知觉变化引起; 另一方面, 运动诱导视盲中“反知觉”现象的特殊性也是研究者关注的问题之一。神经生理机制层面的研究关注早期、晚期皮层在该现象发生时的变化, 采用眼动、脑电等技术对错觉现象发生时程进行测量与评估。文章在总结已有相关研究的基础上进一步指出今后可深入探索的研究方向有：MIB发生的深层机制、作为研究意识神经相关、无意识知觉加工等课题的工具、MIB中的意义性加工与认知冲突等。     

The role of dorsolateral prefrontal function in relationship commitment

Commitment is an important determinant of relationship stability. Previous studies demonstrated that relationship stability is influenced by several personality variables, one of which is conscientiousness. To account for the influence of conscientiousness on relationship stability, we propose a neurological model of commitment. The model assumes that conscientiousness and commitment are influenced by individual differences in anterior and mid-dorsolateral prefrontal (amDLPFC) functioning, and that conscientiousness is a partial mediator of the association between amDLPFC functioning and commitment. Results from two studies with dating couples are consistent with this model. Study 2 suggests that, relative to other conscientiousness facets, self-efficacy is a more likely mediator of the effect of amDLPFC functioning on commitment.     

Neurophysiology and neuroanatomy of smooth pursuit: Lesion studies

Smooth pursuit impairment is recognized clinically by the presence of saccadic tracking of a small object and quantified by reduction in pursuit gain, the ratio of smooth eye movement velocity to the velocity of a foveal target. Correlation of the site of brain lesions, identified by imaging or neuropathological examination, with defective smooth pursuit determines brain structures that are necessary for smooth pursuit. Paretic, low gain, pursuit occurs toward the side of lesions at the junction of the parietal, occipital and temporal lobes (area V5), the frontal eye field and their subcortical projections, including the posterior limb of the internal capsule, the midbrain and the basal pontine nuclei. Paresis of ipsiversive pursuit also results from damage to the ventral paraflocculus and caudal vermis of the cerebellum. Paresis of contraversive pursuit is a feature of damage to the lateral medulla. Retinotopic pursuit paresis consists of low gain pursuit in the visual hemifield contralateral to damage to the optic radiation, striate cortex or area V5. Craniotopic paresis of smooth pursuit consists of impaired smooth eye movement generation contralateral to the orbital midposition after acute unilateral frontal or parietal lobe damage. Omnidirectional saccadic pursuit is a most sensitive sign of bilateral or diffuse cerebral, cerebellar or brainstem disease. The anatomical and physiological bases of defective smooth pursuit are discussed here in the context of the effects of lesion in the human brain.     

Age-Related Differences in Identity Style: A Cross-Sectional Analysis

The Identity Style Inventory–Revised for a Sixth-Grade Reading Level (ISI-6G) was administered to samples of community college students (N = 99) and middle school and high school students (N = 320). Tests of between-groups differences indicated that the college sample had a significantly lower mean diffuse-avoidant score on the ISI-6G than the middle and high school sample. In terms of actual assignment to identity styles, college students were significantly more likely to be classified as informational or normative, while the younger students were more likely to be diffuse-avoidant. The mean ages of participants for each of the three identity styles were compared, and it was found that diffuse-avoidant participants had the lowest mean age (15.54 years), while individuals with an informational orientation had the highest mean age (17.20 years). Results suggest that, in general, identity style evolves with age and maturity and the general trajectory or progression involves movement away from a diffuse-avoidant orientation. Findings are discussed in terms of current knowledge of neurocognitive development during adolescence and early adulthood.     

Medial prefrontal cortex infusions of bupivacaine or AP-5 block extinction of amphetamine conditioned place preference

The present experiments used reversible lesion techniques and intra-mPFC infusions of the n-methyl d-aspartate (NMDA) receptor antagonist d,l-2-amino-5-phosphonovaleric acid (AP-5) to examine the role of the mPFC in extinction of an amphetamine conditioned place preference (CPP). Following initial training and testing for an amphetamine (2 mg/kg) CPP, adult male Long–Evans rats were given extinction trials that were identical to training, except in the absence of peripheral amphetamine injections. Immediately prior to each extinction trial, rats received intra-mPFC infusions of the anesthetic drug bupivacaine (0.75% solution/0.5 μl), AP-5 (1.25, 2.5, 5.0 μg/0.5 μl), or saline. Following extinction training, rats were given a second CPP test session. Rats receiving intra-mPFC infusions of saline displayed extinction of CPP behavior. In contrast, intra-mPFC infusions of bupivacaine or AP-5 (2.5, 5.0 μg) blocked CPP extinction. The findings indicate (1) the mPFC mediates extinction of approach behavior to drug-associated environmental contexts, and (2) NMDA receptor blockade within the mPFC is sufficient to block extinction of amphetamine CPP behavior.     

Hippocampal low-frequency stimulation and chronic mild stress similarly disrupt fear extinction memory in rats

Disruptions of fear extinction-related potentiation of synaptic efficacy in the connection between the hippocampus (HPC) and the medial prefrontal cortex (mPFC) have been shown to impair the recall of extinction memory. This study was undertaken to examine if chronic mild stress (CMS), which is known to alter induction of HPC–mPFC long-term potentiation, would also interfere with both extinction-related HPC–mPFC potentiation and extinction memory. Following fear conditioning (5 tone-shock pairings), rats were submitted to fear extinction (20 tone-alone presentations), which produced an increase in the amplitude of HPC–mPFC field potentials. HPC low-frequency stimulation (LFS), applied immediately after training, suppressed these changes and induced fear return during the retention test (5 tone-alone presentations). CMS, delivered before fear conditioning, did not interfere with fear extinction but blocked the development of extinction-related potentiation in the HPC–mPFC pathway and impaired the recall of extinction. These findings suggest that HPC LFS may provoke metaplastic changes in HPC outputs that may mimic alterations associated with a history of chronic stress.