INTRINSIC VISUAL CORTICAL NEURONS

哺乳动物视觉皮层的一个显著特征是，它由 许多不同的领域通过相互联系而联系在一起。 前向连接是信息从外围设备到 更多的中心区域，而反馈预测传达信息， 从高到低的地区。 我们感兴趣的反馈预测 这些是连接高级皮层区域和初级视觉的神经元 皮层 这样的突出物可以进入皮质内和皮质内。 皮质下投射系统，它们可以在其上施加不同的 影响。 反馈输入在皮质投射中的作用 神经元可能是为了改变纹状体皮层的感受野特性 基于在功能不同的皮层中提取的信息的神经元 区域，并提供视觉刺激的连贯表示 在大脑皮层的早期阶段 相比之下， 皮层下投射系统的反馈输入可以是选择 特定的传入信息或将注意力引导到特定的 点的视野。 潜在的假设是， 不同的功能由不同的电路实现。 因为它 很可能每个传出投射系统，包括局部 interneurons，接收反馈输入的组织中的差异 可能在于输入的强度和亚细胞分布。 该组织可部分确定 激活不同细胞类型的单突触电位。 此外，本发明还提供了一种方法， 突触后反应的差异也可能来自于激活 不同的递质受体，这些受体被认为是 分布在不同的层中，也可能分布在神经元中， 产生不同的预测。 因此，拟议项目的目标 是确定反馈的强度和亚细胞分布 从高级皮质区到中间神经元的输入和不同类型的 初级视皮层的投射神经元，并确定 抑制这些细胞类型的反馈激活的机制。 到 为了实现这一目标，我们将确定，使用顺行神经元示踪 以及光（LM）和电子显微镜（EM）分析的组合， 反馈投射的层状分布和相对强度 从大鼠的次级视觉皮层到初级视觉皮层（目的1）。 以确定 反馈输入到GABA能中间神经元的神经元追踪， 免疫细胞化学将用于识别突触接触下的 LM和EM（目标2）。 顺行和逆行追踪及相关 LM和EM分析将用于确定反馈输入， 投射到次级视觉皮层的条纹状皮层细胞（aim 3）。 一个类似的方法将被用来确定反馈输入到丘 投射神经元（aim 4）。 使用体外细胞内记录 切片，我们将检查是否激活反馈输入eliminate 不同类型的单突触EPSP在不同的细胞类型（目的5）。 为了检测不同细胞的突触后反应是否 通过不同的受体介导，我们将使用细胞内记录， 不同兴奋性氨基酸受体的选择性拮抗剂 6）。

A prominent feature of mammalian visual cortex is that it is composed of many different areas which are linked through reciprocal connections. Forward connections mediate the flow of information from peripheral to more central areas, whereas feedback projections convey information from higher to lower areas. The feedback projections that are of interest here are those that connect higher cortical areas with primary visual cortex. Such projections may have access to both intracortical and subcortical projection systems, on which they may exert different influences. The role of feedback input to corticocortically projecting neurons may be to modify receptive field properties of striate cortical neurons based on information extracted in functionally different cortical areas, and to provide for a coherent representation of a visual stimulus at an early stage in the cortical hierarchy. By contrast, the role of feedback input to subcortical projection systems, may be to select specific afferent information or to direct attention to a particular point of the visual field. The underlying hypothesis is that these different functions are implemented by different circuits. Because it is likely that each of the efferent projections systems, including local interneurons, receive feedback input the difference in the organization may lie in the strength, and the subcellular distribution of inputs. This organization may in part determine the timecourse and amplitude of monosynaptic potentials that activate different cell types. In addition, differences in postsynaptic responses may also arise from the activation of different transmitter receptors that are known to be preferentially distributed in different layers, and possibly also in neurons that give rise to different projections. Thus, the goal of the proposed project is to determine the strength and subcellular distribution of feedback input from higher cortical areas to interneurons and different types of projection neurons in primary visual cortex, and to determine the mechanism(s) that underlay feedback activation of these cell types. To achieve this goal, we will determine, using anterograde neuronal tracing and a combination of light- (LM) and electron microscopic (EM) analyses, the laminar distribution and relative strength of feedback projections from secondary to primary visual cortex in rat (aim 1). To determine feedback input to GABAergic interneurons of neuronal tracing and immunocytochemistry will be used to identify synaptic contacts under the LM and EM (aim 2). Anterograde and retrograde tracing and correlative LM and EM analyses will be employed to determine feedback input to striate cortical cells that project to secondary visual cortex (aim 3). A similar approach will be used to determine feedback input to colliculus projecting neurons (aim 4). Using intracellular recordings in in vitro slices we will examine whether activation of feedback input elicits different types of monosynaptic EPSPs in different cell types (aim 5). To examine whether the postsynaptic responses in different cells are mediated by different receptors we will use intracellular recordings and selective antagonists of different excitatory amino acid receptors (aim 6).