How stopping movement affects working memory
How stopping movement affects working memory
批准号:
8621542
负责人:
Adam Robert Aron
金额:
$18.33万
依托单位国家:
美国
项目类别:
财政年份:
2013
资助国家:
美国
项目状态:
已结题
起止时间:
2013-09-30 至 2015-08-31
关键词:
AffectAreaAuditoryBasal GangliaBehaviorBehavioralBiological ModelsBrainCognitiveCognitive ScienceDataElectrodesElectroencephalographyFigs - dietaryHandImplantInterruptionLegLinkMeasuresMethodsMindModelingMotorMotor CortexMotor Evoked PotentialsMovementParkinson DiseasePatientsPhysiologic pulsePsychiatryPublishingScalp structureShort-Term MemorySignal TransductionSkeletal MuscleSorting - Cell MovementStimulusStructure of subthalamic nucleusSystemSystems TheoryTelephoneTestingTimeTrainingTranscranial magnetic stimulationbasecognitive neuroscienceexperiencefrontal lobehealthy volunteerindexinginnovationmemory processmuscular systemneuromechanismnovelpublic health relevancerelating to nervous systemresearch studysoundtheories
中文摘要
描述(申请人提供):我们都经历过这样的情况,在谈话过程中,我们被一个突出的外部信号(小说)打断,例如窗户被打破。我们很快就适应了小说,然后发现我们的思路,或者更确切地说,我们的工作记忆(WM)被打断了。这项提议检验了这样一种理论,即WM减少的原因之一是因为显著的刺激激活了大脑的运动停止网络,而这个网络对当前活跃的运动和非运动皮质内容具有全局影响。基于我们已发表的和初步的数据,我们提出了以下神经系统模型:a)小说作为停止信号,通过大脑的全局停止网络产生快速的运动停止,b)该网络通过基底节的丘脑底核(STN)实现,c)STN的激活导致对丘脑皮质驱动的广泛抑制脉冲,d)由于所有运动和非运动表征(包括WM)部分地由丘脑皮质驱动维持,存在暂时的中断,表现为WM减少。验证该模型对于更好地理解认知心理学中停止与工作记忆之间的关系,更好地理解帕金森病中的过度停止状态与认知僵化之间的关系,以及提出与精神病学相关的新的分心理论具有深远的意义。我们在帕金森病患者和健康志愿者身上测试了这一模型。在帕金森病患者中,我们将研究停药对WM的影响,同时记录植入的STN电极的局部场电位和额叶皮质的头皮脑电。我们预计STN中的停止诱导的活动将与WM的皮质标志物的减少相对应,从而将假定的全球STN停止信号与WM的减少联系在一起。在健康志愿者中,我们将使用运动皮质的经颅磁刺激作为全球STN停止信号的替代探头。我们预计,用这种方法测量的全球运动抑制程度将与停止信号和小说导致的WM减少相一致。
英文摘要
DESCRIPTION (provided by applicant): We all experience the sort of situation where, during a conversation, we are interrupted by a salient external signal (a 'novel'), e.g. a breaking window. We quickly orient to the novel, and then find that our train of thought, or more specifically our working memory (WM), has been interrupted. This proposal tests the theory that one reason for this WM decrement is because the salient stimulus activates the brain's motor stopping network, and this network has global effects on currently active motor and non-motor cortical contents. Based on our published and preliminary data we advance for the following neural systems model: a) novels act as stop signals, generating a rapid motor stop via the brain's global stopping network, b) this network is implemented via the subthalamic nucleus (STN) of the basal ganglia, c) activation of the STN leads to a widespread pulse of suppression on thalamocortical drive, d) as all motor and non-motor representations (including WM) are partly sustained by thalamocortical drive, there is a temporary interruption which manifests as a WM decrement. Validating this model has far-reaching significance for better understanding the relationship between stopping and WM in cognitive psychology; for better understanding the relation between the 'over-stopped' state in PD and cognitive inflexibility, and for advancing a new theory of distractibility, relevant for psychiatry. We test the model in PD patients and in healthy volunteers. In PD patients we will examine how stopping affects WM while we simultaneously record local field potentials from implanted STN electrodes and scalp EEG from the frontal cortex. We expect that stopping-induced activity in the STN will correspond with reductions in the cortical marker for WM, thus linking the putative global STN stop signal with a decrement in WM. In healthy volunteers we will use Transcranial Magnetic Stimulation of motor cortex as a surrogate probe of the global STN stop signal. We expect that the degree of global motor suppression measured by this method will correspond with the decrement in WM induced by stop signal as well as novels.
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