高级视皮层可塑性:物体和面孔知觉学习综述

复杂刺激的知觉学习是指由训练或经验引起的对物体或者面孔等复杂视觉刺激在知觉上长期稳定的改变,一般认为这反映了大脑高级视皮层的可塑性.对简单刺激知觉学习特性的研究已经揭示了低级视皮层的部分可塑性,但是复杂刺激知觉学习的神经机制目前仍存在争议.本文介绍了知觉学习的理论模型和实验证据,并重点探讨了复杂刺激如物体和面孔知觉学习的特性、神经机制及研究方法.该领域未来需要在复杂刺激知觉学习的持久性、面孔不同属性知觉学习的机制,以及复杂刺激知觉学习的理论模型方面做进一步研究.     

视觉学习与成人大脑的可塑性

我们对视觉特征和客体的分辨与识别能力会随着训练提高,这种现象被称为视知觉学习。对其神经机制的研究使我们更好地理解成人大脑可塑性。回顾了该研究领域的两大核心问题:(1)视知觉学习发生的皮层位置:学习发生在早期信息加工的视皮层,或是涉及决策等认知功能的高级额顶叶区域,抑或是视觉区域到高级认知区域的连接;(2)视知觉学习发生的形式:包括表征增强、表征锐化、易化等多种机制。最后,讨论了神经干预手段在知觉学习领域的应用,并展望该领域未来的研究方向。     

视觉轮廓整合的神经机制

视觉轮廓整合是指视觉系统将视野中的离散元素组合为整体轮廓线的加工过程,是连接初级感觉加工和高级视觉物体知觉间的关键桥梁。对视觉轮廓整合神经机制的研究不仅能促进我们对人类知觉整合的理解,也有助于启发计算科学领域图形整合和分隔算法的改进。然而,轮廓整合的神经机制尚无最终定论。当前的争议主要集中在轮廓整合是基于初级视皮层固有水平连接的产物,还是基于脑区内水平连接及脑区间反馈连接共同作用的产物。本文在回顾这两种理论框架及其研究证据的基础上,对未来的研究问题和方向进行了展望。     

视觉系统中的性别差异

大脑性别差异一直是神经科学领域中的一个热门话题.以前的性别差异研究往往关注与高级认知相关的脑区结构和功能差异,而对低级感知觉系统中的性别差异没有足够的重视.近年来,越来越多的研究结果表明,男性和女性在视知觉功能上也存在着明显的差异.本文首先回顾和梳理了视觉系统中存在性别差异的行为学和神经生物学证据,然后对视觉系统中性别差异的来源提出了两种可能的解释,接着讨论了视知觉功能存在性别差异的进化学意义,最后强调了在感知觉研究中把性别作为一个实验变量的的重要性,并对后续的性别差异研究提出了一些具体的建议.     

双稳态知觉的脑机制

当对视觉输入的信息有多种解释时,人们的知觉状态会在这些解释之间随机切换.目前,这种多稳态或双稳态知觉的神经机制仍处于争论之中.本研究分别以鲁宾花瓶和内克尔立方体两种双稳态图形为对象来研究双稳态知觉在大脑结构上的机制.首先,通过计算两种双稳态知觉的切换频率,发现两者切换频率之间有正相关关系.在此基础上,通过计算两种知觉切换频率与大脑灰质体积的相关性,发现鲁宾花瓶和内克尔立方体图形的切换频率均和右侧额下回的灰质体积存在显著的负相关.本研究表明,不同双稳态知觉之间具有共同的神经基础,这一共同的基础位于右侧额下回,支持了自上而下的加工在双稳态知觉中具有重要的作用.     

睡眠剥夺对认知功能的影响研究进展

睡眠剥夺(sleep deprivation,SD)是一种由于环境或自身原因无法满足正常睡眠的情况.认知是个体认识和理解事物的心理过程,包括对自己与环境的确定、感知、注意、学习和记忆、思维和语言等.认知功能由多个认知域组成,包括记忆、计算、时空间定向、结构能力、执行能力、语言理解和表达及应用等方面.SD可对认知功能产生一定影响,如清醒度、警觉性及注意力下降;感官知觉能力下降;学习记忆能力下降等.SD可能增加氧自由基产生,改变神经递质动态分布,损伤海马结构,诱导异常基因表达以及抑制长时程增强效应,引起脑内神经结构状态紊乱,导致认知功能障碍.本文从SD所致认知障碍的表现形式,认知障碍的可能机制以及SD与神经变性的关系三个方面探讨SD对认知功能的影响.     

应激对机体脑体功能的影响及其生物学机制初探

目的：探讨应激对机体脑体功能的损伤效应及其生物学机制,为应激损伤防护措施的制订提供科学依据。方法：采用束缚应激模型,观察模型动物认知功能、体能、海马LTP、血浆糖皮质激素、心电图、心肌组织结构等指标的变化。结果：应激动物学习记忆能力和运动耐力明显下降,血浆糖皮质激素水平显著升高,海马LTP诱发受到抑制,心电图异常改变,心功能紊乱,心肌组织结构出现病理损伤,心肌细胞凋亡率增加,心肌组织Hsp70表达水平随应激强度增加而逐渐降低。结论：应激诱导机体神经一内分泌功能紊乱,进而导致机体脑体功能损伤。     

连续闪现抑制下对洞的无意识知觉

大量收敛一致的实验证据表明,图形的大范围性质可以由拓扑性质来描述,并且其检测发生在视觉过程的最早期,这些证据几乎全部来自对意识上知觉的研究,而拓扑性质的意识下加工机制尚有待发掘.意识下知觉是人的感官系统客观上接受刺激呈现但主观上没有察觉的知觉,其机制和应用长期以来一直是知觉研究的热点.本文采用了一种双眼竞争的变式——连续闪现抑制,将待检测的刺激图形掩蔽,使之处于意识下状态,考察意识下知觉中拓扑性质的加工."洞的个数"作为一种拓扑性质是本文的研究对象.通过量度被抑制图形从发生变化到被知觉的被抑制时间,或者被试对被抑制的变化图形的正确检测率,我们发现,相比于不变或者各种非拓扑性质变化,意识下知觉中的拓扑性质(洞的个数)的变化会使图形更快、更容易被检测到.本研究揭示了拓扑性质(洞的个数)在意识下知觉中的优先性,将拓扑知觉理论从意识上知觉领域拓展到了意识下知觉领域,为拓扑性质加工的早期性提供了有力的证据;另一方面,本研究也提示了拓扑性质经由皮层下视通路加工处理的可能性.     

昆虫视觉系统平行加工通道研究

许多飞行的昆虫能够借助它们的视觉发现、跟踪、识别、捕获对它们有意义的目标,有些昆虫例如蜜蜂、蝴蝶、蜻蜓等与高等的动物一样,它们也具有空间视觉、运动视觉和颜色视觉,这些视觉信息是如何进行加工的,其加工通道之间的相互关系如何,阐明这些问题对解释视知觉的形成是很重要的.由于昆虫神经系统比人和哺乳动物神经系统简单得多,其神经元的数量亦少得多,因此我们选择了以昆虫的视觉系统为模型系统对此问题进行研究.本文把1986年以来我们对此问题开展行为分析和神经生理学研究所取得的结果以及与此有关的工作综述如下.     

TrkB受体依赖的PV神经元调控小鼠视觉方位辨别能力的机制

神经营养因子-酪氨酸受体激酶B （tyrosine receptor kinase B,TrkB）信号通路在调控初级视皮层（primary visual cortex,V1）兴奋与抑制平衡上发挥着重要的作用,以往的研究揭示了其通过增加兴奋性传递效率来调控皮层兴奋性水平的机制,却并未阐明TrkB受体如何通过抑制系统来调控兴奋与抑制平衡,进而影响视觉皮层功能。为了探讨TrkB信号通路如何特异性地调控最主要的抑制性神经元——PV神经元进而对小鼠视觉皮层功能产生影响,本研究通过病毒特异性地降低V1区的PV神经元上TrkB受体的表达水平,并通过在体多通道电生理手段记录初级视皮层抑制性与兴奋性神经元功能变化,通过行为学实验测试小鼠的方位辨别能力改变。结果表明,初级视觉皮层中的PV抑制性神经元上的TrkB受体表达减少会显著增加兴奋性神经元的反应强度,减弱抑制性神经元与兴奋性神经元的方位辨别能力,增加二者的信噪比,但是小鼠个体水平的方位辨别能力出现下降。这些结果说明,TrkB信号通路并非单纯通过增加靶向PV神经元的兴奋性传递来调控PV神经元的功能,其对神经元信噪比的影响也并非由于抑制系统的增强所致。     

Abnormal Contextual Modulation of Visual Contour Detection in Patients with Schizophrenia

Schizophrenia patients demonstrate perceptual deficits consistent with broad dysfunction in visual context processing. These include poor integration of segments forming visual contours, and reduced visual contrast effects (e.g. weaker orientation-dependent surround suppression, ODSS). Background image context can influence contour perception, as stimuli near the contour affect detection accuracy. Because of ODSS, this contextual modulation depends on the relative orientation between the contour and flanking elements, with parallel flankers impairing contour perception. However in schizophrenia, the impact of abnormal ODSS during contour perception is not clear. It is also unknown whether deficient contour perception marks genetic liability for schizophrenia, or is strictly associated with clinical expression of this disorder. We examined contour detection in 25 adults with schizophrenia, 13 unaffected first-degree biological relatives of schizophrenia patients, and 28 healthy controls. Subjects performed a psychophysics experiment designed to quantify the effect of flanker orientation during contour detection. Overall, patients with schizophrenia showed poorer contour detection performance than relatives or controls. Parallel flankers suppressed and orthogonal flankers enhanced contour detection performance for all groups, but parallel suppression was relatively weaker for schizophrenia patients than healthy controls. Relatives of patients showed equivalent performance with controls. Computational modeling suggested that abnormal contextual modulation in schizophrenia may be explained by suppression that is more broadly tuned for orientation. Abnormal flanker suppression in schizophrenia is consistent with weaker ODSS and/or broader orientation tuning. This work provides the first evidence that such perceptual abnormalities may not be associated with a genetic liability for schizophrenia.     

Neuroanatomical circuitry associated with exploratory eye movement in schizophrenia: a voxel-based morphometric study

Schizophrenic patients present abnormalities in a variety of eye movement tasks. Exploratory eye movement (EEM) dysfunction appears to be particularly specific to schizophrenia. However, the underlying mechanisms of EEM dysfunction in schizophrenia are not clearly understood. To assess the potential neuroanatomical substrates of EEM, we recorded EEM performance and conducted a voxel-based morphometric analysis of gray matter in 33 schizophrenic patients and 29 well matched healthy controls. In schizophrenic patients, decreased responsive search score (RSS) and widespread gray matter density (GMD) reductions were observed. Moreover, the RSS was positively correlated with GMD in distributed brain regions in schizophrenic patients. Furthermore, in schizophrenic patients, some brain regions with neuroanatomical deficits overlapped with some ones associated with RSS. These brain regions constituted an occipito-tempro-frontal circuitry involved in visual information processing and eye movement control, including the left calcarine cortex [Brodmann area (BA) 17], the left cuneus (BA 18), the left superior occipital cortex (BA 18/19), the left superior frontal gyrus (BA 6), the left cerebellum, the right lingual cortex (BA 17/18), the right middle occipital cortex (BA19), the right inferior temporal cortex (BA 37), the right dorsolateral prefrontal cortex (BA 46) and bilateral precentral gyri (BA 6) extending to the frontal eye fields (FEF, BA 8). To our knowledge, we firstly reported empirical evidence that gray matter loss in the occipito-tempro-frontal neuroanatomical circuitry of visual processing system was associated with EEM performance in schizophrenia, which may be helpful for the future effort to reveal the underlying neural mechanisms for EEM disturbances in schizophrenia.     

Spike suppression in a local cortical circuit induced by transcranial magnetic stimulation

Transcranial magnetic stimulation (TMS) noninvasively interferes with human cortical function, and is widely used as an effective technique for probing causal links between neural activity and cognitive function. However, the physiological mechanisms underlying TMS-induced effects on neural activity remain unclear. We examined the mechanism by which TMS disrupts neural activity in a local circuit in early visual cortex using a computational model consisting of conductance-based spiking neurons with excitatory and inhibitory synaptic connections. We found that single-pulse TMS suppressed spiking activity in a local circuit model, disrupting the population response. Spike suppression was observed when TMS was applied to the local circuit within a limited time window after the local circuit received sensory afferent input, as observed in experiments investigating suppression of visual perception with TMS targeting early visual cortex. Quantitative analyses revealed that the magnitude of suppression was significantly larger for synaptically-connected neurons than for isolated individual neurons, suggesting that intracortical inhibitory synaptic coupling also plays an important role in TMS-induced suppression. A conventional local circuit model of early visual cortex explained only the early period of visual suppression observed in experiments. However, models either involving strong recurrent excitatory synaptic connections or sustained excitatory input were able to reproduce the late period of visual suppression. These results suggest that TMS targeting early visual cortex disrupts functionally distinct neural signals, possibly corresponding to feedforward and recurrent information processing, by imposing inhibitory effects through intracortical inhibitory synaptic connections.     

Single units and conscious vision.

Figures that can be seen in more than one way are invaluable tools for the study of the neural basis of visual awareness, because such stimuli permit the dissociation of the neural responses that underlie what we perceive at any given time from those forming the sensory representation of a visual pattern. To study the former type of responses, monkeys were subjected to binocular rivalry, and the response of neurons in a number of different visual areas was studied while the animals reported their alternating percepts by pulling levers. Perception-related modulations of neural activity were found to occur to different extents in different cortical visual areas. The cells that were affected by suppression were almost exclusively binocular, and their proportion was found to increase in the higher processing stages of the visual system. The strongest correlations between neural activity and perception were observed in the visual areas of the temporal lobe. A strikingly large number of neurons in the early visual areas remained active during the perceptual suppression of the stimulus, a finding suggesting that conscious visual perception might be mediated by only a subset of the cells exhibiting stimulus selective responses. These physiological findings, together with a number of recent psychophysical studies, offer a new explanation of the phenomenon of binocular rivalry. Indeed, rivalry has long been considered to be closely linked with binocular fusion and stereopsis, and the sequences of dominance and suppression have been viewed as the result of competition between the two monocular channels. The physiological data presented here are incompatible with this interpretation. Rather than reflecting interocular competition, the rivalry is most probably between the two different central neural representations generated by the dichoptically presented stimuli. The mechanisms of rivalry are probably the same as, or very similar to, those underlying multistable perception in general, and further physiological studies might reveal much about the neural mechanisms of our perceptual organization.     

Reduced Crowding and Poor Contour Detection in Schizophrenia Are Consistent with Weak Surround Inhibition

Background

Detection of visual contours (strings of small oriented elements) is markedly poor in schizophrenia. This has previously been attributed to an inability to group local information across space into a global percept. Here, we show that this failure actually originates from a combination of poor encoding of local orientation and abnormal processing of visual context.

Methods

We measured the ability of observers with schizophrenia to localise contours embedded in backgrounds of differently oriented elements (either randomly oriented, near-parallel or near-perpendicular to the contour). In addition, we measured patients’ ability to process local orientation information (i.e., report the orientation of an individual element) for both isolated and crowded elements (i.e., presented with nearby distractors).

Results

While patients are poor at detecting contours amongst randomly oriented elements, they are proportionally less disrupted (compared to unaffected controls) when contour and surrounding elements have similar orientations (near-parallel condition). In addition, patients are poor at reporting the orientation of an individual element but, again, are less prone to interference from nearby distractors, a phenomenon known as visual crowding.

Conclusions

We suggest that patients’ poor performance at contour perception arises not as a consequence of an “integration deficit” but from a combination of reduced sensitivity to local orientation and abnormalities in contextual processing. We propose that this is a consequence of abnormal gain control, a phenomenon that has been implicated in orientation-selectivity as well as surround suppression.     

Portrait of visual cortical circuits for generating neural oscillation dynamics

The mouse primary visual cortex (V1) has emerged as a classical system to study neural circuit mechanisms underlying visual function and plasticity. A variety of efferent-afferent neuronal connections exists within the V1 and between the V1 and higher visual cortical areas or thalamic nuclei, indicating that the V1 system is more than a mere receiver in information processing. Sensory representations in the V1 are dynamically correlated with neural activity oscillations that are distributed across different cortical layers in an input-dependent manner. Circuits consisting of excitatory pyramidal cells (PCs) and inhibitory interneurons (INs) are the basis for generating neural oscillations. In general, INs are clustered with their adjacent PCs to form specific microcircuits that gate or filter the neural information. The interaction between these two cell populations has to be coordinated within a local circuit in order to preserve neural coding schemes and maintain excitation–inhibition (E–I) balance. Phasic alternations of the E–I balance can dynamically regulate temporal rhythms of neural oscillation. Accumulating experimental evidence suggests that the two major sub-types of INs, parvalbumin-expressing (PV⁺) cells and somatostatin-expressing (SOM⁺) INs, are active in controlling slow and fast oscillations, respectively, in the mouse V1. The review summarizes recent experimental findings on elucidating cellular or circuitry mechanisms for the generation of neural oscillations with distinct rhythms in either developing or matured mouse V1, mainly focusing on visual relaying circuits and distinct local inhibitory circuits.     

Cortical Contributions to Saccadic Suppression

The stability of visual perception is partly maintained by saccadic suppression: the selective reduction of visual sensitivity that accompanies rapid eye movements. The neural mechanisms responsible for this reduced perisaccadic visibility remain unknown, but the Lateral Geniculate Nucleus (LGN) has been proposed as a likely site. Our data show, however, that the saccadic suppression of a target flashed in the right visual hemifield increased with an increase in background luminance in the left visual hemifield. Because each LGN only receives retinal input from a single hemifield, this hemifield interaction cannot be explained solely on the basis of neural mechanisms operating in the LGN. Instead, this suggests that saccadic suppression must involve processing in higher level cortical areas that have access to a considerable part of the ipsilateral hemifield.     

The neural basis of centre-surround interactions in visual motion processing

Perception of a moving visual stimulus can be suppressed or enhanced by surrounding context in adjacent parts of the visual field. We studied the neural processes underlying such contextual modulation with fMRI. We selected motion selective regions of interest (ROI) in the occipital and parietal lobes with sufficiently well defined topography to preclude direct activation by the surround. BOLD signal in the ROIs was suppressed when surround motion direction matched central stimulus direction, and increased when it was opposite. With the exception of hMT+/V5, inserting a gap between the stimulus and the surround abolished surround modulation. This dissociation between hMT+/V5 and other motion selective regions prompted us to ask whether motion perception is closely linked to processing in hMT+/V5, or reflects the net activity across all motion selective cortex. The motion aftereffect (MAE) provided a measure of motion perception, and the same stimulus configurations that were used in the fMRI experiments served as adapters. Using a linear model, we found that the MAE was predicted more accurately by the BOLD signal in hMT+/V5 than it was by the BOLD signal in other motion selective regions. However, a substantial improvement in prediction accuracy could be achieved by using the net activity across all motion selective cortex as a predictor, suggesting the overall conclusion that visual motion perception depends upon the integration of activity across different areas of visual cortex.     

Blinking suppresses the neural response to unchanging retinal stimulation

Blinks profoundly interrupt visual input but are rarely noticed, perhaps because of blink suppression, a visual-sensitivity loss that begins immediately prior to blink onset. Blink suppression is thought to result from an extra-retinal signal that is associated with the blink motor command and may act to attenuate the sensory consequences of the motor action. However, the neural mechanisms underlying this phenomenon remain unclear. They are challenging to study because any brain-activity changes resulting from an extra-retinal signal associated with the blink motor command are potentially masked by profound neural-activity changes caused by the retinal-illumination reduction that results from occlusion of the pupil by the eyelid. Here, we distinguished direct top-down effects of blink-associated motor signals on cortical activity from purely mechanical or optical effects of blinking on visual input by combining pupil-independent retinal stimulation with functional MRI (fMRI) in humans. Even though retinal illumination was kept constant during blinks, we found that blinking nevertheless suppressed activity in visual cortex and in areas of parietal and prefrontal cortex previously associated with awareness of environmental change. Our findings demonstrate active top-down modulation of visual processing during blinking, suggesting a possible mechanism by which blinks go unnoticed.