Hupé J M, James A C, Girard P, Bullier J
Cerveau et Vision, Institut National de la Santé et de la Recherche Médicale U371, 69675 Bron Cedex, France.
J Neurophysiol. 2001 Jan;85(1):146-63. doi: 10.1152/jn.2001.85.1.146.
We analyzed the extracellular responses of 70 V1 neurons (recorded in 3 anesthetized macaque monkeys) to a single oriented line segment (or bar) placed within the cell classical receptive field (RF), or center of the RF. These responses could be modulated when rings of bars were placed entirely outside, but around the RF (the "near" surround region), as described in previous studies. Suppression was the main effect. The response was enhanced for 12 neurons when orthogonal bars in the surround were presented instead of bars having the same orientation as the center bar. This orientation contrast property is possibly involved in the mediation of perceptual pop-out. The enhancement was delayed compared with the onset of the response by about 40 ms. We also observed a suppression originating specifically from the flanks of the surround. This "side-inhibition," significant for nine neurons, was delayed by about 20 ms. We tested whether these center/surround interactions in V1 depend on feedback connections from area V2. V2 was inactivated by GABA injections. We used devices made of six micropipettes to inactivate the convergent zone from V2 to V1. We could reliably inactivate a 2- to 4-mm-wide region of V2. Inactivation of V2 had no effect on the center/surround interactions of V1 neurons, even those that were delayed. Therefore the center/surround interactions of V1 neurons that might be involved in pop-out do not appear to depend on feedback connections from V2, at least in the anesthetized monkey. We conclude that these properties are probably shaped by long-range connections within V1 or depend on other feedback connections. The main effect of V2 inactivation was a decrease of the response to the single bar for about 10% of V1 neurons. The decrease was delayed by <20 ms after the response onset. Even the earliest neurons to respond could be affected by the feedback from V2. Together with the results on feedback connections from MT (previous paper), these findings show that feedback connections potentiate the responses to stimulation of the RF center and are recruited very early for the treatment of visual information.
我们分析了70个V1神经元(记录于3只麻醉的猕猴)对置于细胞经典感受野(RF)内或RF中心的单个定向线段(或条带)的细胞外反应。如先前研究所述,当条带环完全置于RF之外但围绕RF(“近”周边区域)时,这些反应可能会受到调制。抑制是主要效应。当周边呈现正交条带而非与中心条带方向相同的条带时,12个神经元的反应增强。这种方向对比度特性可能参与了感知弹出的介导过程。与反应开始相比,增强延迟了约40毫秒。我们还观察到一种特别源自周边侧翼的抑制。这种“侧向抑制”对9个神经元具有显著性,延迟约20毫秒。我们测试了V1中的这些中心/周边相互作用是否依赖于来自V2区域的反馈连接。通过注射GABA使V2失活。我们使用由六个微吸管制成的装置使从V2到V1的汇聚区域失活。我们能够可靠地使V2中2至4毫米宽的区域失活。V2失活对V1神经元的中心/周边相互作用没有影响,即使是那些延迟的相互作用。因此,可能参与弹出过程的V1神经元的中心/周边相互作用似乎不依赖于来自V2的反馈连接,至少在麻醉的猴子中是这样。我们得出结论,这些特性可能是由V1内的长程连接塑造的,或者依赖于其他反馈连接。V2失活的主要效应是约10%的V1神经元对单个条带的反应减少。减少在反应开始后延迟<20毫秒。即使是最早做出反应的神经元也可能受到来自V2的反馈的影响。连同关于来自MT的反馈连接的结果(前一篇论文),这些发现表明反馈连接增强了对RF中心刺激的反应,并且在视觉信息处理中很早就被招募。