The origins of neuronal correlations in cerebral cortex

项目摘要 在这里，我们建议使用协同混合来彻底描述大脑皮层成对相关性的起源。 在老鼠和猕猴身上的实验方法、行为和计算。我们将澄清 正常化的机制基础，并测试我们的假设，即皮质成对相关性的变化 和其他特征来自于正在进行的大脑皮层计算。在目标1中，我们将从神经元群体中记录 在训练有素、行为正常的猴子的颞叶中部视觉区域检验成对棘波的假说 视觉刺激开始时的相关性、伽马振荡和瞬变反应部分源于 使神经元反应正常化的电路的动力学。这些测试需要精确的测量 这在老鼠身上是不可行的。相反，目标2和3中的实验解决了不可行的问题。 在猴子身上。在目标2中，我们将通过使用双光子激光来开发小鼠视觉皮质的可达性 扫描显微镜和多电极阵列综合测量之间的关系 V1神经元群体的归一化和成对相关性，并衡量内部空间分离 大脑皮层会影响这种关系。最后，在目标3中，我们将确定特定细胞类的贡献 小鼠V1的归一化和成对相关。我们记录了锥体神经元的活动和 在正常化过程中，三类特征最全面的皮质中间神经元(VIP、SST和PV)。我们 然后，我将分别操作这些细胞类的活动，以揭示随比率变化的角色 兴奋和抑制在驾驶正常化中发挥作用。通过这种方式，我们将确定这些神经元所扮演的角色 在改变兴奋性神经元池内的成对相关性方面。这三个目标的结果将会平分秋色 一起使用一族新的动态、递归的标准化电路模型来形式化假设 归一化强制实施成对关联和其他活动签名，并将使用实验数据 约束和优化这些模型。

Project Summary Here, we propose to thoroughly characterize the origins of pairwise correlations in cortex using a synergistic mix of experimental methodologies, behavior, and computation in mice and macaques. We will elucidate the mechanistic underpinnings of normalization and test our hypothesis that changes in cortical pairwise correlations and other signature arise from ongoing cortical computations. In Aim 1 we will record from populations of neurons in the middle temporal visual area of trained, behaving monkeys to test the hypothesis that pairwise spike correlations, gamma oscillation and transient responses at the onset of visual stimuli arise in part from the dynamics of the circuits that normalize neuronal responses. These tests require measurements with a precision that is not feasible in mice. Conversely, the experiments in Aim 2 and 3 address questions that are not feasible in monkeys. In Aim 2 we will exploit the accessibility of mouse visual cortex by using both two-photon laser scanning microscopy and multielectrode arrays to comprehensively measure the relationship between normalization and pairwise correlations in populations of V1 neurons and measure how spatial separation within cerebral cortex affects that relationship. Finally, in Aim 3 we will establish the contributions of specific cell classes to normalization and pairwise correlations in mouse V1. We record the activity of pyramidal neurons and the three most thoroughly characterized classes of cortical interneuron (VIP, SST and PV) during normalization. We will then separately manipulate the activity of these cells classes to revealing the role that changes to the ratio of excitation and inhibition play in driving normalization. In this way, we will establish the role these neurons play in changing pairwise correlations within the excitatory pool of neurons. Results from all three Aims will be tied together using a new family of dynamic, recurrent circuit models of normalization to formalize the hypothesis that normalization imposes pairwise correlations and other activity signatures, and will use experimental data to constrain and refine these models.