DEVELOPMENTAL REGULATION OF POTENTIATION IN CORTEX

视觉皮层的神经元容易受到快速的功能性和 结构组织对改变的感觉输入的反应， 损伤 然而，这种可塑性的确切机制尚不清楚， 已经使用了几个模型来描述这种现象。 其中一 模型是Bienenstock，库珀和芒罗模型，其中包括 需要在会前活动和会后活动之间有时间上的重叠， 突触后细胞 Fregnac等人（1994）描述了一种可能的相关性 对于该体外模型，称为协方差诱导增强（CIP）， 在视觉皮层的第二或第三层。 CIP可以在视觉上引起 然而，无论是年轻的还是成年的动物， CIP的诱导机制经历了戏剧性的发展变化。 而CIP诱导在成人皮层需要激活NMDA 受体，CIP在年轻的皮质可以诱导独立的 激活NMDA受体。无论是成年人还是年轻人 然而，在皮层，CIP诱导依赖于 胞内Ca 2+。 这表明Ca 2+的另一种机制 年轻大脑皮层的信号 本提案的目标是 确定在年轻人中引起CIP的机制 皮层，并确定1）是否这种平行的Ca 2+信号（在 NMDAR）与可塑性级联解耦 在发育过程中，2）机制中的发育转换是否 CIP诱导是由于总有效Ca 2+信号的变化 通过激活NMDAR递送到神经元，或3）是否 在可塑性级联反应中，Ca 2+信号的下游发生变化 在成人中。 我将使用一系列电生理/ 药理学分析和Ca 2+成像，以确定 Ca 2+诱导CIP在年轻的皮质，以及 成人大脑皮层发育开关的本质

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.