Neural mechanisms of visual contrast sensitivity

项目摘要 这项研究计划的主要目标是了解神经元网络如何进行通信 来产生视觉感知。这些知识将有助于生物工程师和临床医生在开发 新的设备和治疗方法，为患者的知觉障碍。了解视觉如何在 恒河猴是一种视觉与人类相似的动物，它将使我们更接近于了解 健康和疾病状态下的人类视觉生理学。本研究的具体目标是三个 初级视觉皮层（V1）对视觉对比敏感度的不同贡献。所有 目的是使用类似的方法：一种新的，可逆的神经元失活系统， 同时进行定量行为测量。这些测量将揭示信号是如何路由的 通过视觉系统来控制行为。第一个目标是确定有多少基线噪声， V1有助于感知报告的可变性。这一目标将通过抑制V1活性来实现， 训练来报告低对比度视觉刺激的猴子。在一些试验中，没有刺激 猴子必须猜一猜是否是。一个关键问题是抑制V1活性 防止猴子猜测刺激出现了，而实际上没有。第二个目标是 以确定绕过V1的视觉通路是否足以调节猴子的行为， 报道我们将通过测试猴子检测旨在激活神经元的刺激的能力来实现这一目标。 绕过V1的通路。如果猴子在V1的活动受到抑制时能看到这些刺激， 控制实验的预测得到证实，我们将知道，旁路V1的途径可以介导 对比度检测第三个目的是确定V1活动的方面是否比前馈 截击对于刺激检测是必要的。我们将通过测量猴子的阈值来实现这一目标， 当V1区的活动受到抑制时，检测V2区的电微刺激。共同完成 这些目标将回答关于V1区在刺激检测中的作用的重要和突出的问题。 这些问题不能用经典技术充分解决， 我们将用来完成这些目标是一个重要的技术贡献的拟议工作。

PROJECT SUMMARY The major objective of this research program is to understand how networks of neurons communicate to produce visual perception. This knowledge will be useful to bioengineers and clinicians in the development of new devices and treatments for patients with perceptual disorders. Understanding how vision works in rhesus monkeys, an animal whose vision is similar to humans', will bring us closer to understanding the physiology of human vision in states of health and disease. The Specific Aims of this study target three different components of how the primary visual cortex (V1) contributes to visual contrast sensitivity. All of the Aims use a similar methodology: a novel, reversible system for neuronal inactivation combined with simultaneous quantitative behavioral measurement. These measurements will reveal how signals are routed through the visual system to control behavior. The first Aim is to determine how much of the baseline noise in V1 contributes to the variability of perceptual reports. This Aim will be achieved by suppressing V1 activity in a monkey trained to report the presentation of a low-contrast visual stimulus. On some trials, no stimulus is shown and the monkey must guess whether one was. A key question is whether suppression of V1 activity prevents the monkey from guessing that a stimulus was presented when none, in fact, was. The second Aim is to determine whether the visual pathways that bypass V1 are sufficient to mediate the monkeys' behavioral reports. We will achieve this Aim by testing the monkeys' ability to detect stimuli designed to activate the neural pathways that bypass V1. If the monkey can see these stimuli when activity in V1 is suppressed, and if the predictions of control experiments are confirmed, we will know that the pathways that bypass V1 can mediate contrast detection. The third Aim is to determine whether aspects of V1 activity other than the feedforward volley are necessary for stimulus detection. We will achieve this Aim by measuring the monkeys' threshold for detecting electrical microstimulation of area V2 when activity in V1 is suppressed. Together, completion of these Aims will answer important and outstanding questions about the role of area V1 in stimulus detection. These questions cannot be adequately addressed with classical techniques, and the inactivation technique that we will use to complete these Aims is an important technical contribution of the proposed work.