The molecular mechanisms underlying neuron-glia interaction during long-term memory formation

记忆形成过程中神经元-神经胶质相互作用的分子机制尚不清楚。先前我们发现，细胞粘附分子克林贡（Klg）在神经元和胶质细胞中均有表达，并且Klg介导的神经元-胶质相互作用的训练依赖性增加是形成长期记忆（LTM）所必需的。我们还发现Klg调节神经胶质基因的表达，这是LTM形成所必需的。在这项研究中，我们发现了一种新的神经胶质调节LTM形成的机制。我们确定Klg介导特定类型的神经元和神经胶质之间的相互作用，并发现这些相互作用增加了神经胶质转录因子Repo的表达。反过来，Repo激活神经胶质基因表达，防止ltm诱导的细胞死亡。

The molecular mechanisms underlying neuron-glia interaction during memory formation are poorly understood. Previously we discovered that a cell adhesion molecule, Klingon (Klg), is expressed in both neurons and glia, and a training-dependent increase in Klg-mediated neuron-glia interactions is required to form long-term memory (LTM). We also found that Klg modulates glial gene expression, which is required for LTM formation. In this study we identified a novel mechanism for glial regulation of LTM formation. We determined that Klg mediates interactions between specific types of neurons and glia, and found that these interactions increase expression of a glial transcription factor, Repo. Repo, in turn, activates a glial gene expression that functions to prevent LTM-induced cell death.