What are the effects of severe visual impairment on the cortical organization and connectivity of primary visual cortex?
What are the effects of severe visual impairment on the cortical organization and connectivity of primary visual cortex?
复制标题
DOI：
10.3389/neuro.05.030.2009
复制
发表时间：
2009-12-23
影响因子：
2.9
通讯作者：
Krubitzer, Leah
中科院分区：
文献类型：
--
作者：
Larsen, DeLaine D.;Luu, Julie D.;Krubitzer, Leah
在缺乏功能性视杆(GNAT-/-)，但锥体功能正常的小鼠中，观察了初级视觉区域(V1)的组织和连接。由于小鼠是夜间活动的，正常行为几乎完全依赖视杆视觉，因此本研究中使用的GNAT-/-小鼠被认为是功能性盲鼠。我们的目标是确定这些小鼠的视觉皮质是否重组，并检查可能有助于重组的神经解剖学联系。我们发现，V1中的大多数神经元对听觉或听觉、体感和/或视觉刺激的某种组合有反应。我们还发现，GNAT-/-小鼠V1的皮质联系与正常动物相似，但即使在正常动物中，从听觉皮质(AC)到V1的输入也很少。一个重要的观察结果是，V1的皮质下输入大部分来自正常投射到V1的丘脑核团，如外侧膝状体(LG)、外侧后核(LP)和外侧背核(LD)。然而，V1也接受了一些来自丘脑前核、腹后核、腹侧核和后核的皮质下异常传入。虽然从少量锥体产生的视觉似乎足以维持大多数正常连接的模式，但稀疏的异常丘脑输入到VI，现有的来自AC的输入，以及可能的异常输入到LG和LP可能是导致V1功能组织变化的原因。
The organization and connections of the primary visual area (V1) were examined in mice that lacked functional rods (Gnat-/-), but had normal cone function. Because mice are nocturnal and rely almost exclusively on rod vision for normal behaviors, the Gnat-/- mice used in the present study are considered functionally blind. Our goal was to determine if visual cortex is reorganized in these mice, and to examine the neuroanatomical connections that may subserve reorganization. We found that most neurons in V1 responded to auditory, or some combination of auditory, somatosensory, and/or visual stimulation. We also determined that cortical connections of V1 in Gnat-/- mice were similar to those in normal animals, but even in normal animals, there is sparse input from auditory cortex (AC) to V1. An important observation was that most of the subcortical inputs to V1 were from thalamic nuclei that normally project to V1 such as the lateral geniculate (LG), lateral posterior (LP), and lateral dorsal (LD) nuclei. However, V1 also received some abnormal subcortical inputs from the anterior thalamic nuclei, the ventral posterior, the ventral lateral and the posterior nuclei. While the vision generated from the small number of cones appears to be sufficient to maintain most of the patterns of normal connectivity, the sparse abnormal thalamic inputs to VI, existing inputs from AC, and possibly abnormal inputs to LG and LP may be responsible for generating the alterations in the functional organization of V1.