DEVELOPMENT OF SYNAPTIC PLASTICITY IN THE VISUAL CORTEX

大脑皮层突触改变其信号效率的动态能力被认为是学习和经验依赖性修饰的许多方面的基础。介导活动依赖性突触可塑性的细胞和分子过程，包括视觉皮层。视觉皮层突触信号的这种活动依赖性变化，无论是短暂的还是持续的，也被认为有助于视觉输入的动态皮层处理，从而影响视觉感知、认知表现、技能学习和功能性视觉皮层突触网络的发育重组和完善。然而，这些形式的突触可塑性的发育调节受到较少的关注。在视觉皮层，在神经元结构、功能和行为水平上已经证明了环境养育条件、周围感觉缺陷（如视网膜病变、斜视或形式视觉障碍）的显著后果。我们利用新皮层突触可塑性模型（DCM模型）来表征成熟和新生动物视觉新皮层中负责一种功能性突触可塑性的细胞过程。我们之前已经发现，这种形式的突触可塑性，或协方差诱导-增强（CIP），发生在成人视觉皮层的单个锥体神经元中，它是由n -甲基- d天冬氨酸（NMDA）谷氨酸受体的激活和突触后细胞内钙的增加触发的。与成熟的视觉皮层相比，新生儿中CIP的诱导更为强烈。然而，触发突触电位的细胞机制经历了一个戏剧性的发育开关。触发机制从nmda受体非依赖性转变为nmda受体依赖性过程。我们假设了代谢性谷氨酸受体电压检测和电压门控钙通道之间耦合机制的发育控制改变。我们将通过结合电生理技术和高分辨率钙成像技术，确定这种发育调节可塑性的分子巧合检测器和信号级联。

The dynamic capacity for synapses in the cerebral cortex to change their signaling efficiency is thought to underlie many aspects of learning and experience-dependent modification. The cellular and molecular processes that mediate activity-dependent synaptic plasticity including the visual cortex. Such activity-dependent changes in synaptic signaling in the visual cortex, whether of a transient or sustained nature also have been suggested to contribute to dynamic cortical processing of visual input with consequences for visual perception, cognitive performance, skill- learning and developmental re-organization and refinement of functional visual cortical synaptic networks. However, the developmental regulation of these forms of synaptic plasticity has received less attention. In the visual cortex, dramatic consequences of environmental rearing conditions, peripheral sensory deficits such as retinal lesions, strabismus or form vision disturbances have been demonstrated at the level of neuronal structure, function and behavior. We utilize a model of neocortical synaptic plasticity (the DCM model) to characterize the cellular processes that are responsible for a type of functional synaptic plasticity in the visual neo-cortex of mature and neonatal animals. We have previously found that this form of synaptic plasticity, or covariance-induced- potentiation (CIP), occurs in individual pyramidal neurons of the adult visual cortex and it is triggered by activation of the N-methyl-D aspartate (NMDA) glutamate receptors and a rise in postsynaptic intracellular calcium. The induction of CIP is considerably more robust in the neonatal versus the mature visual cortex. However, the cellular mechanism for triggering the synaptic potential undergoes a dramatic developmental switch. The triggering mechanism switches from an NMDA-receptor independent to an NMDA-receptor dependent process. We have posited a developmentally controlled alteration in the coupling mechanism between voltage detection by metabotropic glutamate receptors and voltage-gated calcium channels, respectively. We will identify the molecular coincidence detector and signaling cascade for this type of developmentally regulated plasticity by combining electrophysiological techniques with high-resolution calcium imaging.