PLASTICITY OF SYNAPTIC MEMBRANE SPECIALIZATIONS

神经元的可塑性对于神经元回路中的补偿是重要的 损伤后，老化中的神经元磨损， 成年期和连接的发展组织。 虽然 发芽恢复突触接触的数量被认为是 神经系统可塑性的一种常见形式， 突触部位现在似乎也是一种重要的机制， 浦肯野细胞传入神经阻滞后立即反应。 本研究 解决了其他神经元是否也有这种潜力的问题 作为一种产物， 每个目标神经元上突触后接触面积的恒定性。 这项研究旨在通过以下方式来测试这一守恒原理： 定量分析大脑的另外两个区域，即 上级颈神经节优势神经元和颗粒细胞 海马体的一部分。 在主要传入神经减少后， 这两个靶神经元之间的关系， 目标神经元上的输入位点和个体的平均大小 将定量突触后膜特化。 中的值 一系列不同的减少水平将被用来定义是否 每个神经元上的总接触面积保持不变， 每个目标神经元上的传入接触的数量。 结果 将建立：（1）是否其他神经元（除了浦肯野细胞）可能是 能够通过快速重新分配 大分子的剩余受体膜位点，（2）是否有 支持一种假设，即快速可塑性的机制是基于 对靶位点的内在控制和（3）突触后位点是否 反过来诱导传入神经产生更多的突触囊泡和更大的 突触前总接触面积

Plasticity of neurons is important for compensation in neuronal circuitry following lesions, neuronal attrition in aging, environmental influences in adulthood and developmental organization of connectivity. Although sprouting to restore the number of synaptic contacts is considered the common form of plasticity in the nervous system, changes in the size of synaptic sites now also appear to be an important mechanism for almost immediate response following Purkinje cell deafferentation. This study addresses the question of whether other neurons also have this potential for rapid alteration in the size of remaining synaptic sites as a product of a constancy in total postsynaptic contact area on each target neuron. The study is designed to test for this conservation principle by quantitative analysis of two other regions of the brain, namely the predominent neurons of the superior cervical ganglion and the granule cells of the hippocampus. Following reductions in the principal afferents to these two target neurons, the relationship between the number of afferent input sites on target neurons and the average size of individual postsynaptic membrane specializations will be quantitated. The values from a series of different reduction levels will be used to define whether the total area of contact on each neuron remains constant regardless of the amount of afferent contacts on each of the target neurons. The results will establish: (1) whether other neurons (besides Purkinje cells) may be able to re-organize connectivity through rapid redistribution of macromolecules for remaining receptor membrane sites, (2) whether there is support for a hypothesis that a mechanism of rapid plasticity is based on intrinsic control over target sites and (3) whether the post-synaptic sites in turn induce the afferents to produce more synaptic vesicles and a larger total presynaptic contact area.