言语学习引起的脑功能和结构变化

文章系统介绍了言语学习引起的脑功能和结构可塑性变化研究的最新进展,例如：第二语言的词汇——语义学习引起的脑功能变化主要受熟练程度的影响,而句法学习引起的脑功能变化主要受获得年龄的影响;实验室言语训练可以引起语言加工相关区域激活增强或减弱,以及出现新的激活区域;第二语言学习导致了左侧顶下皮层灰质密度增加。此外,文章还总结了言语学习的脑成像研究中常用的实验范式,并提出了有待于进一步解决的关键问题     

关于早期经验对脑影响的实验研究

近年来,强调早期教育(或训练)对儿童智力和行为发展重要性的文章很多,其理论根据是:早期教育(或训练)是一种早期经验,早期经验对个体后来的发展和学习具有重要作用。动物方面的实验研究证明,早期经验对脑解剖学和脑化学有明显影响,这些结果正在为早期教育理论提供生理上的根据。本文准备介绍有关研究情况,希望对于发展心理学的研究有参考价值。     

第二语言学习与脑可塑性

脑可塑性指人脑会因为环境刺激、认知需求和行为经验而产生功能或结构改变。近10年来的单双语者对比和语言训练研究结果表明, 不论儿童、青年或老年人, 第二语言学习和使用都能改变其脑运行模式并带来相应结构变化, 包括灰质(GM)体积和白质(WM)密度增加, 且长期持续的双语经验还能形成认知优势, 帮助抵制由老化导致的负面认知影响。基于脑可塑性概念及其研究证据, 从双语经验与语言训练两方面, 对比分析了长期和短期第二语言学习引起脑功能或结构变化及其内在机制, 并对未来相关研究进行了展望。     

延迟满足——一个值得在我国开展的研究计划

本文以文献回顾为出发点,阐述“延迟满足”之基本研究范式及研究新趋势,并以此为基础,构思一个在中国各地开展的研究计划.具体来说,此计划包括六点建议:(一)实验研究以密斯(Mischel)的基本研究范式为蓝本,(二)在研究设计上结合问卷测量与实验研究,(三)细致地比较个人测试和群体测试的异同,(四)致力进行“发展向度”的研究,(五)制订吻合理论建构及本土处境的“延迟满足”测量问卷,(六)从“延迟满足”过渡至“满足于过程”.     

国外对基于问题的学习的研究

作为可以改变传统教育中学生被动接受、死学习、缺乏实践和创新的新型教学模式,基于问题的学习模式(PBL)值得我们探索研究。本文对于基于问题的学习进行如下论述:(1)起源,(2)国外对定义、模式、特征等方面的研究,(3)对于多位国外学者研究的总结。     

学习与记忆的机制

学习和记忆是脑的最高级机能之一。对学习与记忆规律及其机制的探讨,一直是脑科学研究的重要课题,也是心理学中实验研究最多的一个领域,它需要心理学、神经生理学、脑化学等多种学科的合作。目前的研究是从两个方向进行的:一个是通过心理学的方法,从思想和情感的内部表现对大脑进行研究,另一个是运用神经生理学的方法,即研究神经系统的物理学、化学和生物学侧面。建立在近代实验科学基础上的对学习记忆机制的研究,还是最近二十几年的事情。随着神经生理、神经生化、分子生物学等学     

统计学习的认知神经机制及其与语言的关系

统计学习是指个体在连续刺激流中发现转移概率等统计规律的过程, 在Saffran等(1996)的经典婴儿语音切分研究中首次被提出。大量研究证实了统计学习的普遍存在, 近期学界开始关注统计学习的特异性及其对认知的影响, 尤其是从学习过程及其特异性两个方面阐述统计学习的认知神经机制并揭示其和语言的交互作用。未来应从脑和行为的多模态数据视角, 丰富统计学习结果的行为和神经指标, 考察不同类型统计学习过程的动态神经活动模式, 建立统计学习行为和脑的关联, 深化对统计学习认知神经机制的认识, 在统计学习与语言交互作用的基础上, 从成人二语学习切入结合音乐统计学习训练探讨促进语言学习的统计学习干预手段。     

老年人的脑可塑性:来自认知训练的证据

老年人大脑结构和功能衰退是其认知功能下降的重要原因。然而,老年人的大脑仍然保持了一定的可塑性。随着神经影像技术的发展,大量研究发现认知训练能够对老年人的大脑结构和功能产生积极影响:(1)在脑结构方面,表现为大脑皮层灰质体积增加、白质神经纤维连接增强;(2)在进行认知任务时,表现为脑功能网络发生重组;(3)在静息态脑功能方面,表现为脑自发活动功能性重组以及功能连接增强。未来的认知训练研究需要考察老年人大脑可塑性存在个体差异的多种影响因素,并通过纵向追踪研究来探讨大脑可塑性的保持性和迁移效应。     

学习与脑可塑性的研究进展及其教育意义

脑可塑性是指脑在外界环境和经验的作用下不断塑造其结构和功能的能力.本文阐述了神经科学与认知神经科学关于学习影响动物脑与人脑结构与功能的研究进展.研究表明,学习与经验可以改变脑皮层的厚度与树突的结构,增加树突棘的数量,修饰其形状,对脑的功能代表区产生影响.学习与脑可塑性的多层面研究为理解学习的本质规律以及教育研究与实践提供重要的启示.     

聋人早期手语经验对脑功能及结构的塑造作用

语言经验对脑功能和结构发展有重要的塑造作用。然而, 目前的相关证据主要来自对脑损伤导致的失语症病人的语言康复、第二语言学习以及针对成人读者进行的语言训练等方面的研究。幼儿时期的早期语言经验对脑结构与功能发展的影响更加重要, 但直接的研究证据却相当缺乏。本文提出一个研究设想, 拟综合使用多种脑成像技术, 系统探讨有早期手语经验和无早期手语经验的聋人个体在脑皮层语言功能的组织及脑结构发育的差异, 包括语言任务中大脑语言区的激活模式, 静息状态下脑功能联结的默认网络特征, 脑皮层灰质密度, 以及神经纤维束发育状况等, 揭示早期语言经验对大脑功能和结构发育的塑造作用。     

Plasticity of nonneuronal brain tissue: roles in developmental disorders

Neuronal and nonneuronal plasticity are both affected by environmental and experiential factors. Remodeling of existing neurons induced by such factors has been observed throughout the brain, and includes alterations in dendritic field dimensions, synaptogenesis, and synaptic morphology. The brain loci affected by these plastic neuronal changes are dependent on the type of experience and learning. Increased neurogenesis in the hippocampal dentate gyrus is a well-documented response to environmental complexity ("enrichment") and learning. Exposure to challenging experiences and learning opportunities also alters existing glial cells (i.e., astrocytes and oligodendrocytes), and up-regulates gliogenesis, in the cerebral cortex and cerebellum. Such glial plasticity often parallels neuronal remodeling in both time and place, and this enhanced morphological synergism may be important for optimizing the functional interaction between glial cells and neurons. Aberrant structural plasticity of nonneuronal elements is a contributing factor, as is aberrant neuron plasticity, to neurological and developmental disorders such as epilepsy, autism, and mental retardation (i.e., fragile X syndrome). Some of these nonneuronal pathologies include abnormal cerebral and cerebellar white matter and myelin-related proteins in autism; abnormal myelin basic protein in fragile X syndrome (FXS); and abnormal astrocytes in autism, FXS, and epilepsy. A number of recent studies demonstrate the possibility of using environmental and experiential intervention to reduce or ameliorate some of the neuronal and nonneuronal abnormalities, as well as behavioral deficits, present in these neurological and developmental disorders.     

情绪神经回路的可塑性

从两个方面介绍了近年来关于情绪神经回路可塑性的研究进展：（1）情绪神经回路中各主要脑区（包括前额叶、杏仁核等）的可塑性及其相互影响;（2）情绪神经回路可塑性的影响因素,包括情绪学习、早期环境和经历以及抚养者的情绪状态等。文章最后还对情绪神经回路可塑性的研究方法及未来的研究方向进行了探讨     

Visuomotor Adaptation and Proprioceptive Recalibration

ABSTRACT

Motor learning, in particular motor adaptation, is driven by information from multiple senses. For example, when arm control is faulty, vision, touch, and proprioception can all report on the arm's movements and help guide the adjustments necessary for correcting motor error. In recent years we have learned a lot about how the brain integrates information from multiple senses for the purpose of perception. However, less is known about how multisensory data guide motor learning. Most models of, and studies on, motor learning focus almost exclusively on the ensuing changes in motor performance without exploring the implications on sensory plasticity. Nor do they consider how discrepancies in sensory information (e.g., vision and proprioception) related to hand position may affect motor learning. Here, we discuss research from our lab and others that shows how motor learning paradigms affect proprioceptive estimates of hand position, and how even the mere discrepancy between visual and proprioceptive feedback can affect learning and plasticity. Our results suggest that sensorimotor learning mechanisms do not exclusively rely on motor plasticity and motor memory, and that sensory plasticity, in particular proprioceptive recalibration, plays a unique and important role in motor learning.     

MAP2 and synaptophysin protein expression following motor learning suggests dynamic regulation and distinct alterations coinciding with synaptogenesis

Learning a new motor skill can induce neuronal plasticity in rats. Within motor cortex, learning-induced plasticity includes dendritic reorganization, synaptogenesis, and changes in synapse morphology. Behavioral studies have demonstrated that learning requires protein synthesis. It is likely that some of the proteins synthesized during learning are involved in, or the result of, learning-induced structural plasticity. We predicted the expression of proteins involved in neural plasticity would be altered in a learning dependent fashion. Long-Evans rats were trained on a series of motor tasks that varied in complexity, so that the effects of activity could be teased apart from the effects of learning. The motor cortices were examined for MAP2 and synaptophysin protein using Western blotting and immunohistochemistry. Western blotting revealed that expression of MAP2 was not detectably influenced by learning, whereas synaptophysin expression increased on day 1, 3, and 5 of complex motor skill learning. Expression of MAP2 does not seem to indicate difficulty of task or duration of training time, whereas increases in synaptophysin expression, which appear diffusely across the cortex, seem to be correlated with the first 5 days of motor skill learning. Similar findings with GAP-43 suggest the change in synaptophysin may coincide with synapse formation. Immunohistochemistry did not reveal any localized changes in protein expression. These data indicate a difference in learning-induced expression in the mammalian brain compared to reports in the literature, which have often focused on stimulation to induce alterations in protein expression.     

Long-term plasticity of intrinsic excitability: learning rules and mechanisms

Spatio-temporal configurations of distributed activity in the brain is thought to contribute to the coding of neuronal information and synaptic contacts between nerve cells could play a central role in the formation of privileged pathways of activity. Synaptic plasticity is not the exclusive mode of regulation of information processing in the brain, and persistent regulations of ionic conductances in some specialized neuronal areas such as the dendrites, the cell body, and the axon could also modulate, in the long-term, the propagation of neuronal information. Persistent changes in intrinsic excitability have been reported in several brain areas in which activity is elevated during a classical conditioning. The role of synaptic activity seems to be a determinant in the induction, but the learning rules and the underlying mechanisms remain to be defined. We discuss here the role of synaptic activity in the induction of intrinsic plasticity in cortical, hippocampal, and cerebellar neurons. Activation of glutamate receptors initiates a long-term modification in neuronal excitability that may represent a parallel, synergistic substrate for learning and memory. Similar to synaptic plasticity, long-lasting intrinsic plasticity appears to be bidirectional and to express a certain level of input or cell specificity. These nonsynaptic forms of plasticity affect the signal propagation in the axon, the dendrites, and the soma. They not only share common learning rules and induction pathways with the better-known synaptic plasticity such as NMDA receptor dependent LTP and LTD, but also contribute in synergy with these synaptic changes to the formation of a coherent engram.     

中枢N-甲基-D-天冬氨酸受体在应激所致行为改变中的作用

应激所致行为效应的脑机制研究是目前生理心理学研究的热点领域。近年来,对于参与应激所致行为效应的神经递质研究从5-HT、多巴胺和去甲肾上腺素的范畴,逐渐发展到关注脑内含量最为丰富的谷氨酸能神经元所产生的兴奋性递质,包括谷氨酸、天冬氨酸及其相应受体NMDAR可能在应激性行为效应的中枢机制中的作用。近十年来的研究表明,中枢NMDAR是学习记忆的关键物质,在兴奋性突触传递、突触可塑性和脑发育过程中扮演重要的角色。不同类型的应激能导致动物的与行为密切相关脑区如杏仁核,海马的兴奋性氨基酸及NMDAR数量增多,活性增高。突触间隙增多的兴奋性氨基酸与NMDAR结合后,通过激活NMDAR促进糖皮质激素的相关性释放,共同产生的兴奋毒性作用引起上述脑区的神经元细胞缺失和变性;或干扰其他中枢神经递质在动物行为的脑内奖赏机制中的正常功能;或通过持续激活NMDAR,导致细胞内Ca2＋超载,损害其信号传导途径下游的蛋白激酶级联反应,使其底物蛋白的磷酸化或去磷酸化作用发生改变,影响突触可塑性和神经细胞间的信号传递,导致动物出现相应的行为障碍。应激前给动物的上述脑区注射NMDAR阻滞剂,可以减轻动物的应激性焦虑和抑郁行为。而NMDAR依赖性LTP下游途径的新信号分子,神经颗粒素,参与了脑内多种蛋白信号传导,可能是应激性行为效应的另一重要中枢机制。     

Cellular memory in spinal nociceptive circuitry

Besides transmitting and processing, neurons may also store information for prolonged periods of time (e.g. by use-dependent change in synaptic strength). In 1966 long-term potentiation (LTP) of synaptic transmission was discovered in the hippocampus, an area implicated in learning and memory. Recent studies show that similar mechanisms apply to pain pathways, at least in the spinal cord, and may account for some forms of clinical problems like hyperalgesia, allodynia, and deafferentation pain states, such as phantom pain. In this review, we briefly summarize key aspects of synaptic plasticity known from the brain and in the spinal cord. Then we describe and discuss related changes in spinal nociceptive neurons based on results from our own laboratory.     

Hippocampal tauopathy in tau transgenic mice coincides with impaired hippocampus-dependent learning and memory, and attenuated late-phase long-term depression of synaptic transmission

We evaluated various forms of hippocampus-dependent learning and memory, and hippocampal synaptic plasticity in THY-Tau22 transgenic mice, a murine tauopathy model that expresses double-mutated 4-repeat human tau, and shows neuropathological tau hyperphosphorylation and aggregation throughout the brain. Focussing on hippocampus, immunohistochemical studies in aged THY-Tau22 mice revealed prominent hyper- and abnormal phosphorylation of tau in CA1 region, and an increase in glial fibrillary acidic protein (GFAP) in hippocampus, but without signs of neuronal loss. These mice displayed spatial, social, and contextual learning and memory defects that could not be reduced to subtle neuromotor disability. The behavioral defects coincided with changes in hippocampal synaptic functioning and plasticity as measured in paired-pulse and novel long-term depression protocols. These results indicate that hippocampal tauopathy without neuronal cell loss can impair neural and behavioral plasticity, and further show that transgenic mice, such as the THY-Tau22 strain, might be useful for preclinical research on tauopathy pathogenesis and possible treatment.     

Mouse vocal communication system: Are ultrasounds learned or innate?

Mouse ultrasonic vocalizations (USVs) are often used as behavioral readouts of internal states, to measure effects of social and pharmacological manipulations, and for behavioral phenotyping of mouse models for neuropsychiatric and neurodegenerative disorders. However, little is known about the neurobiological mechanisms of rodent USV production. Here we discuss the available data to assess whether male mouse song behavior and the supporting brain circuits resemble those of known vocal non-learning or vocal learning species. Recent neurobiology studies have demonstrated that the mouse USV brain system includes motor cortex and striatal regions, and that the vocal motor cortex sends a direct sparse projection to the brainstem vocal motor nucleus ambiguous, a projection previously thought be unique to humans among mammals. Recent behavioral studies have reported opposing conclusions on mouse vocal plasticity, including vocal ontogeny changes in USVs over early development that might not be explained by innate maturation processes, evidence for and against a role for auditory feedback in developing and maintaining normal mouse USVs, and evidence for and against limited vocal imitation of song pitch. To reconcile these findings, we suggest that the trait of vocal learning may not be dichotomous but encompass a broad spectrum of behavioral and neural traits we call the continuum hypothesis, and that mice possess some of the traits associated with a capacity for limited vocal learning.