NEUROBEHAVIORAL RELATIONS IN SENESCENT HIPPOCAMPUS

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 这项研究计划的目的是了解正常衰老导致的记忆损伤的基础。在过去的19年里，我们在细胞和网络水平上发现了空间记忆缺陷与海马区连接性和可塑性的年龄相关变化之间的联系。虽然对海马体的经验关注是合理的，因为这种结构在记忆中起着关键作用，但上游皮质-海马区输入的变化对这些与年龄相关的行为缺陷的影响程度尚不清楚。裂孔周围皮质处于腹侧视觉处理流的最高水平。它将多模式感觉信息传递到海马体，与海马体广泛相互联系，本身对记忆至关重要。因此，它是否将退化的信息传递给老化的海马体，导致视觉感知或刺激联想的缺陷，是目前拨款中解决的一个主要问题。一个补充的问题是，在老化过程中，海马区连接和可塑性机制的崩溃是否会导致新皮质区域之间的关联结合缺陷，从而降低情景记忆的稳定性。了解衰老过程是如何改变这些结构之间的双向相互作用的，以及网络交流中的这种失败可能如何导致行为缺陷，可以为所有年龄段的记忆的神经机制提供洞察。

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.