Essential Cortical Mechanisms for Working Memory

工作记忆的基本皮质机制

基本信息

批准号：
10676983
负责人：
CLAYTON E CURTIS
金额：
$ 38.81万
依托单位：
NEW YORK UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2006
资助国家：
美国
起止时间：
2006-04-05 至 2024-07-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10676983
关键词：
Affect Area Beds Behavioral Brain Brain imaging Clinical Code Cognition Cognitive remediation Compensation Computer Models Data Diagnosis Elderly Failure Feedback Goals Human Impaired cognition Impairment Individual Individual Differences Knowledge Link Longevity Maintenance Maps Memory Memory Loss Memory impairment Mental disorders Mission Modeling Neurobiology Neurologic Noise Occipital lobe Outcome Parietal Parietal Lobe Pathologic Pattern Performance Population Population Dynamics Prefrontal Cortex Property Psychiatric therapeutic procedure Public Health Publishing Research Research Personnel Resources Role Short-Term Memory Signal Transduction Stimulus Structure Techniques Testing Transcranial magnetic stimulation United States National Institutes of Health Visual Visual Cortex Visual Fields Work area striata frontal lobe innovation insight intraparietal sulcus member neglect nervous system disorder neural neurobiological mechanism neuroimaging neuromechanism neuropsychiatric disorder resilience retinotopic stem support network theories

项目摘要

Despite that many failures of high-level cognition are due to the limited resources that support working memory (WM), we know almost nothing about the neural mechanisms underlying these WM limitations, nor the strategies employed to mitigate the limits of our memory. This gap in our knowledge is critical because a host of neuropsychiatric disorders suffer from WM dysfunction. Our long-term goal is to understand the mechanisms by which WM representations are limited and how these limitations can be mitigated. Our overall hypothesis is two-fold. 1) A network of cortical areas support WM, where the population dynamics within distinct nodes encode and maintain stimulus features and mnemonic strategies. 2) The amount of available WM resources is proportional to some properties of the node’s population (e.g., size) within which these dynamics reside. The central aim of the project is to dissect the cortical network that supports WM, causally linking canonical WM mechanisms to visual field maps in frontal, parietal, and occipital cortex, and identifying the underlying mechanisms that limit WM. The rationale for the proposed research is that, as we better understand the neural mechanisms of WM, a strong theoretical framework will emerge within which strategies for understanding individual differences and treating cognitive dysfunction will emerge. Using functional brain imaging, transcranial magnetic stimulation (TMS), and computational modeling, we test our central hypothesis by pursuing three specific aims. 1) The structure of the neural populations that encode WM representations constrain the precision, capacity, and resilience of WM; 2) Prefrontal and parietal cortex make critical but distinct contributions to WM; and 3) Early visual cortex is necessary for the maintenance of visual WM. Strong preliminary data demonstrate the feasibility of proposed work as well as initial support for the hypotheses. Under Aim 1, the size of retinotopically-defined frontal and parietal visual field maps predicts both individual differences in the precision of WM and the degree to which TMS affects WM. Under Aim 2, TMS to parietal cortex impacts memory precision, while perturbation of frontal cortex affected the strategic allocation of WM resources. Under Aim 3, TMS to primary visual cortex causes a loss of precision for remembered items encoded in the perturbed portion of the visual field, supporting a model by which visual cortex acts as a workspace for top-down feedback signals during WM. Overall, the proposed work will generate data needed to dissect the cortical network that supports WM, causally linking canonical WM mechanisms to visual field maps in frontal, parietal, and occipital cortex, and identifying the underlying mechanisms that limit WM. The approach is innovative because it combines computational neuroimaging, modeling, and causal techniques to directly test WM theories within a test bed of well-defined topographically organized populations. The proposed research is significant because it is expected to provide key insights into the causes of WM limits in humans, in addition to providing new targets for cognitive remediation in psychiatric, neurologic, and geriatric populations.

尽管许多高级认知的失败是由于支持工作记忆的资源有限（WM），我们对这些 WM 限制背后的神经机制几乎一无所知，也不了解用于减轻我们记忆限制的策略至关重要，因为主机。的神经精神疾病患有 WM 功能障碍，我们的长期目标是了解其机制。 WM 表示受到哪些限制以及如何减轻这些限制是我们的总体假设。 1) 皮质区域网络支持 WM，其中不同节点内的群体动态。编码和维护刺激特征和助记策略 2) 可用的 WM 资源量是。与这些动态所在的节点群体的某些属性（例如大小）成正比。该项目的中心目标是剖析支持 WM 的皮质网络，将典型的 WM 因果联系起来额叶、顶叶和枕叶皮层视野图的机制，并识别潜在的限制 WM 的机制是，随着我们更好地了解神经机制。 WM 的机制，一个强大的理论框架将出现，其中理解策略利用功能性脑成像，个体差异和治疗认知功能障碍将会出现。经颅磁刺激（TMS）和计算模型，我们通过以下方式测试我们的中心假设追求三个具体目标 1）编码 WM 表示的神经群体的结构。限制 WM 的精确度、容量和弹性；2) 前额叶和顶叶皮层至关重要，但对 WM 的显着贡献；以及 3) 早期视觉皮层对于维持强视觉 WM 是必要的。初步数据证明了拟议工作的可行性以及对假设的初步支持。在目标 1 下，视网膜局部定义的额叶和顶叶视野图的大小可以预测个体的 WM 精度的差异以及 TMS 对 WM 的影响程度在目标 2 下，TMS 对顶叶的影响。皮层影响记忆精度，而额叶皮层的扰动影响 WM 的策略分配在目标 3 下，对初级视觉皮层的 TMS 会导致记忆项目的准确性下降。编码在视野的扰动部分中，支持视觉皮层充当视觉皮层的模型总体而言，拟议的工作将生成所需的数据。剖析支持 WM 的皮质网络，将规范 WM 机制与视野图因果联系起来额叶、顶叶和枕叶皮质，并确定限制 WM 的潜在机制。之所以具有创新性，是因为它结合了计算神经成像、建模和因果技术，直接在明确的地形组织人群的测试床上测试 WM 理论。研究意义重大，因为它有望为人类 WM 限制的原因提供重要见解，除了为精神病学、神经学和老年人群的认知矫正提供新目标之外。

项目成果

期刊论文数量（16）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Common neural mechanisms supporting spatial working memory, attention and motor intention.

DOI：
10.1016/j.neuropsychologia.2010.12.020
发表时间：
2011-05
期刊：
Neuropsychologia
影响因子：
2.6
作者：
Ikkai A;Curtis CE
通讯作者：
Curtis CE

Differential roles of the frontal and parietal cortices in the control of saccades.

额叶和顶叶皮质在眼跳控制中的不同作用。

DOI：
10.1016/j.bandc.2013.06.005
发表时间：
2013
期刊：
Brain and cognition
影响因子：
2.5
作者：
Bender,Julia;Tark,Kyeong-Jin;Reuter,Benedikt;Kathmann,Norbert;Curtis,ClaytonE
通讯作者：
Curtis,ClaytonE

Prioritized maps of space in human frontoparietal cortex.

DOI：
10.1523/jneurosci.3810-12.2012
发表时间：
2012-11-28
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
0
作者：
Jerde TA;Merriam EP;Riggall AC;Hedges JH;Curtis CE
通讯作者：
Curtis CE

The search for the neural mechanisms of the set size effect.

寻找集合大小效应的神经机制。