Visually Driven Activation in Macaque Areas V2 and V3 without Input from the Primary Visual Cortex
Visually Driven Activation in Macaque Areas V2 and V3 without Input from the Primary Visual Cortex
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DOI：
10.1371/journal.pone.0005527
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发表时间：
2009-05-13
期刊：
影响因子：
3.7
通讯作者：
Smirnakis, Stelios M.
中科院分区：
文献类型：
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作者：
Schmid, Michael C.;Panagiotaropoulos, Theofanis;Smirnakis, Stelios M.
在初级视皮层(V1)形成局灶性病变为研究膝纹外通路在激活纹外视皮层中的作用提供了机会。先前的研究表明，猕猴V2和V3区超过95%的神经元在可逆冷却V1后停止放电[1，2，3]。然而，还没有关于恒河猴永久性V1损伤后V2、V3区长期恢复的研究报告。在这里，我们使用猕猴功能磁共振成像来研究V1区损伤后1-22个月内V2区、V3区的活动模式。我们发现，视觉驱动的大胆反应持续存在于V2和V3区的V1病变投影区(LPZ)内，但与病变前水平相比，强度平均降低了70%。从V1损伤后一个月开始，随着时间的推移监测LPZ的活动，没有发现BOLD信号幅度的系统性变化。令人惊讶的是，LPZ内V2、V3区的视网膜组织仍与非损毁半球相似，提示V2、V3区LPZ的激活不是附近(非损毁)V1皮质输入的结果。多单位活动的电生理学记录证实了大胆的观察：即使视觉刺激完全包含在V1病变引起的暗点内，视觉驱动的多单位反应也可以在V2 LPZ内诱发。将刺激限制在完整的半视野内，在V2、V3 LPZ内没有产生显著的大胆调制。我们的结论是，观察到的活动模式在很大程度上是由平行的、V1旁路的皮质下通路调节的，这些通路可以在没有V1输入的情况下激活V2和V3区。这种途径可能会导致失明的行为现象。
Creating focal lesions in primary visual cortex (V1) provides an opportunity to study the role of extra-geniculo-striate pathways for activating extrastriate visual cortex. Previous studies have shown that more than 95% of neurons in macaque area V2 and V3 stop firing after reversibly cooling V1 [1,2,3]. However, no studies on long term recovery in areas V2, V3 following permanent V1 lesions have been reported in the macaque. Here we use macaque fMRI to study area V2, V3 activity patterns from 1 to 22 months after lesioning area V1. We find that visually driven BOLD responses persist inside the V1-lesion projection zones (LPZ) of areas V2 and V3, but are reduced in strength by similar to 70%, on average, compared to prelesion levels. Monitoring the LPZ activity over time starting one month following the V1 lesion did not reveal systematic changes in BOLD signal amplitude. Surprisingly, the retinotopic organization inside the LPZ of areas V2, V3 remained similar to that of the non-lesioned hemisphere, suggesting that LPZ activation in V2, V3 is not the result of input arising from nearby (non-lesioned) V1 cortex. Electrophysiology recordings of multi-unit activity corroborated the BOLD observations: visually driven multi-unit responses could be elicited inside the V2 LPZ, even when the visual stimulus was entirely contained within the scotoma induced by the V1 lesion. Restricting the stimulus to the intact visual hemi-field produced no significant BOLD modulation inside the V2, V3 LPZs. We conclude that the observed activity patterns are largely mediated by parallel, V1-bypassing, subcortical pathways that can activate areas V2 and V3 in the absence of V1 input. Such pathways may contribute to the behavioral phenomenon of blindsight.