Neocortical areas comprised of multiple neuronal circuits which are encoded with innumerable advanced cognitive tasks. Studies focused on neuronal network and synaptic plasticity has hypothesized that every specific neuron and the circuit process the explicit essential information for the specific tasks. However, the structure of these circuits and the involved critical neurons remain to be elucidated. Considering our previous studies, showing the specificity of rat postrhinal cortex comprising specific neuronal circuit for encoding both the learning and recall of shape discrimination through a fast neurotransmitter release from the transduced neurons, here we have demonstrated that postsynaptic neurons in two distinct areas, perirhinal cortex and the ventral temporal association areas are required for the specific visual shape discriminations learning. The constitutively active PKC was delivered into neuronal cells in postrhinal cortex, and the animals were allowed to learn the new shape discriminations, and then the silencing siRNA was delivered into postsynaptic neurons in either perirhinal cortex or ventral temporal association areas, using a novel technology for gene transfer into connected neurons. We observed that expression of the siRNA caused the deficits in visual performance, via blocking the activity in the neurons, as displayed by activity-dependent gene imaging, and also subsequently obstructed the activation of specific signaling pathways required for further learning, and dendritic protein synthesis and CREB. Thus, ratifying the conclusion that the two parallel circuits are both required for the visual shape discrimination learning.

新皮质区域由多个神经元回路组成，这些回路由无数高级认知任务编码。专注于神经元网络和突触可塑性的研究假设每个特定的神经元和电路都为特定任务处理明确的基本信息。然而，这些电路的结构和所涉及的关键神经元仍有待阐明。考虑到我们之前的研究，显示了大鼠鼻后皮层的特异性，包括特定的神经元回路，通过从转导的神经元中快速释放神经递质来编码形状辨别的学习和回忆，在这里我们已经证明了两个不同区域的突触后神经元，特定的视觉形状辨别学习需要鼻周皮层和腹侧颞叶关联区域。组成型激活的 PKC 被传递到鼻后皮层的神经元细胞中，让动物学习新的形状辨别能力，然后使用一种新技术将沉默的 siRNA 传递到鼻周皮层或腹侧颞叶联合区域的突触后神经元中。基因转移到连接的神经元中。我们观察到 siRNA 的表达通过阻断神经元中的活动导致视觉性能缺陷，正如活动依赖性基因成像所显示的那样，并且随后还阻碍了进一步学习和树突蛋白合成所需的特定信号通路的激活和 CREB。因此，