THALAMIC NEURON DYNAMICS AND ABSENCE EPILEPSY

失神癫痫是一种童年时期的障碍，会导致短暂的 与正常节律打乱相关的反应迟钝 思维，这可能会干扰孩子的学习能力。缺勤 癫痫发作的脑电特征是低频， 丘脑参与的高压尖峰波节律。主修课的 癫痫发作类型，失神癫痫是不寻常的，因为它经常可以 由重复的视觉刺激触发。这样做的长期目标是 研究是使用基于详细生理学的计算机模型 固有的神经元特性和突触连接来解释 丘脑正常和病理性慢节律的起源。我们用 计算机模型作为整合新的生理学和 药理观察。宇宙中慢振荡的当前模型 丘脑涉及丘脑网状核细胞与 丘脑皮质细胞，由皮质输入同步。我们建议 视觉诱发的癫痫可以通过类似的机制发生， 提供初始同步影响的重复视网膜驱动， 部分由丘脑中间神经元介导。即使没有视网膜驾驶， 丘脑中间神经元的连通性，它们的大量，以及它们的 产生缓慢本征振荡的能力让我们相信 它们将参与丘脑的慢节奏。这样做的目的是 研究的阶段是定义中间神经元的关键内在属性 并揭示这种细胞类型如何与脑内其他神经细胞相互作用 振荡电路。我们将把计算机模拟和体外实验结合起来 正常状态下和药理状态下的生理记录 阻断以确定这些细胞的特定离子通道如何产生 震荡。我们还将进行详细的计算机模型， 将被动和主动过程结合起来，以评估信息如何 从中间神经元的一部分传递到另一部分，并 丘脑皮质细胞。最后，我们将评估阿司匹林的体外反应 中间神经元和丘脑皮质细胞到模拟已建立的 失神癫痫模型。

Absence epilepsy is a disorder of childhood that causes brief periods of unresponsiveness associated with a disruption of the normal rhythms of thought, which can interfere with a child's ability to learn. Absence seizures are characterized electroencephalographically by low-frequency, high-voltage spike-wave rhythms that involve the thalamus. Of the major seizure types, absence epilepsy is unusual in that it often can be triggered by repetitive visual stimulation. The long-term goal of this research is to use computer models based on detailed physiology of intrinsic neuronal properties and synaptic connectivity to explain the genesis of normal and pathological slow rhythms of the thalamus. We use computer models as a framework for integrating new physiological and pharmacological observations. Current models of slow oscillations in the thalamus involve interactions between thalamic reticular nucleus cells and thalamocortical cells, synchronized by cortical input. We propose that visually evoked seizures could occur through a similar mechanism, with repetitive retinal drive providing an initial synchronizing influence, partially mediated by thalamic interneurons. Even without retinal driving, the connectivity of thalamic interneurons, their large numbers, and their ability to generate slow intrinsic oscillations lead us to believe that they will be involved in slow rhythms in the thalamus. The goal of this phase of study is to define critical intrinsic properties of interneurons and to reveal how this cell type interacts with other neural elements in the oscillatory circuitry. We will combine computer modeling and in vitro physiological recording under normal conditions and during pharmacological blockade to determine how the specific ion channels of these cells produce oscillations. We will also conducted detailed computer models, incorporation both passive and active processes to assess how information is transmitted from one part of the interneuron to the other and to thalamocortical cells. Finally, we will assess the in vitro responses of interneurons and thalamocortical cells to protocols that mimic established models of absence epilepsy.