NEUROBEHAVIORAL RELATIONS IN SENESCENT HIPPOCAMPUS

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目及 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 这项研究计划的目的是了解正常衰老导致的记忆障碍的基础。 在过去的19年里，我们发现了空间记忆缺陷与海马连接性和可塑性在细胞和网络水平上的年龄相关变化之间的联系。 虽然海马的经验重点是合理的，因为这个结构在记忆中的关键作用，上游皮质海马输入的变化在多大程度上有助于这些年龄相关的行为缺陷是未知的。 嗅周皮层是腹侧视觉处理流的最高层。 它将多模态的感觉信息传递到海马体，与海马体广泛地连接，并且本身对记忆至关重要。 它是否会将退化的信息传递到老年海马体，导致视觉感知或刺激关联的缺陷，因此是本研究资助的一个主要问题。 一个补充问题是，在老化过程中，海马回路的连接性和可塑性机制是否会导致新皮层区域之间的关联性结合缺陷，从而降低情景记忆的稳定性。 了解这些结构之间的双向相互作用如何被衰老过程改变，以及网络通信中的这种故障如何导致行为缺陷，可以为所有年龄段的记忆神经机制提供见解。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The objective of this research program is to understand the basis of memory impairments that result from normal aging. Over the past 19 years we have discovered links between spatial memory deficits and age-related changes in hippocampal connectivity and plasticity at the cellular and network levels. While empirical focus on the hippocampus is justified because of this structures critical role in memory, the extent to which changes in upstream cortico-hippocampal inputs contribute to these age-related behavioral deficits is unknown. The perirhinal cortex is at the highest level of the ventral visual processing stream. It carries polymodal sensory information to the hippocampus, is extensively reciprocally connected with it, and is critical for memory in its own right. Whether it transmits degraded information to the aged hippocampus, resulting in deficits in visual perception or stimulus associations is thus a major question addressed in the present grant. A complementary question is whether the breakdown during aging in the connectivity and plasticity mechanisms of hippocampal circuits leads to defective associative binding among neocortical areas, and hence less robust stabilization of episodic memories. Understanding how the bidirectional interactions between these structures are altered by the aging process, and how such failures in network communication may contribute to behavioral deficits, could provide insights into the neural mechanisms of memory at all ages.