DEVELOPMENTAL REGULATION OF POTENTIATION IN CORTEX

视皮层的神经元容易受到快速的功能和 对改变的感觉输入和反应的结构组织 受伤。然而，这种可塑性的确切机制尚不清楚， 有几个模型被用来描述这种现象。这其中的一个 Models是Bienenstock，Cooper和Munro模型，它结合了 Pre和Pre中活动之间的时间重叠要求 突触后细胞。Fregnac等人(1994)描述了一个可能的相关性 对于这个体外模型，称为协方差诱导增强(CIP)， 在视觉皮质的II/III层。CIP可以在视觉上引发 然而，来自幼年和成年动物的皮质切片， CIP的诱导机制经历了一个戏剧性的发展变化。 而在成年大脑皮质诱导CIP需要激活NMDA 受体，CIP在幼年皮质中可以被诱导而不依赖于 激活NMDA受体。无论是成年人还是年轻人 然而，大脑皮层CIP的诱导依赖于 细胞内钙离子。这表明了钙离子的另一种机制 幼年皮层中的信号。这项建议的目标是 确定导致年轻人CIP的机制 并确定1)这种平行的钙信号(在 添加到NMDAR)从塑性级联中解耦 在发育过程中，2)发育机制中的发育开关 CIP的诱导是由于总有效钙信号的变化 通过激活NMDAR传递给神经元或3) 在塑性级联中，变化发生在钙信号的下游 在成人身上。我将使用一系列的电生理/ 药理分析和钙显像法确定黄连的来源 在幼年皮层诱导CIP所需的钙离子，以及 成人大脑皮层发育开关的性质。

The neurons of the visual cortex are susceptible to rapid functional and structural organization in response to altered sensory inputs and injury. The precise mechanisms of this plasticity are unknown, however, several models have been used to describe this phenomena. One of these models is the Bienenstock, Cooper and Munro model, which incorporates a requirement for temporal overlap between activity in the pre- and postsynaptic cell. Fregnac et al.(1994) described a possible correlate for this model in vitro, termed covariance-induced potentiation (CIP), in layer II/III of the visual cortex. CIP can be elicited in visual cortical slices from both young and adult animals, however, the mechanisms of induction of CIP undergo a dramatic developmental change. Whereas CIP induction in the adult cortex requires activation of NMDA receptors, CIP in the young cortex can be induced independent of activation of the NMDA receptors. In both the adult and the young cortex, however, CIP induction is dependent on an increase in intracellular Ca2+. This suggests an alternative mechanism for the Ca2+ signal in young cortex. The objectives of this proposal are to determine the mechanisms responsible for CIP induction in the young cortex, and to determine 1) whether this parallel Ca2+ signal (in addition to the NMDARs) becomes uncoupled from the plasticity cascade during development, 2)whether the developmental switch in the mechanisms of CIP induction is due to a change in the total effective Ca2+ signal delivered to the neuron through activation of NMDARs or 3) whether the change occurs downstream from the Ca2+ signal in the plasticity cascade in the adult. I will employ a series of electrophysiological/ pharmacological analyses and Ca2+ imaging to determine the source of Ca2+ necessary for the induction of CIP in young cortex, as well as the nature of the developmental switch in the adult cortex.