Path integration (PI) is a highly conserved, self-motion-based navigation strategy. Since the discovery of grid cells in the medial entorhinal cortex, neurophysiological data and computational models have suggested that these neurons serve PI. However, more direct empirical evidence supporting this hypothesis has been missing due to a lack of selective manipulations of grid cell activity and suitable behavioral assessments. Here we report that selective disruption of grid cell activity in mice can be achieved by removing NMDA glutamate receptors from the retro-hippocampal region and that disrupted grid cell firing accounts for impaired PI performance. Notably, the genetic manipulation did not affect the activity of other spatially selective cells in the medial entorhinal cortex and the hippocampus. By directly linking grid cell activity to PI, these results contribute to a better understanding of how grid cells support navigation and spatial memory.

中文翻译：

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网格细胞放电中断的小鼠路径整合受损。

路径集成（PI）是一种高度保守的基于自我运动的导航策略。自在内侧内嗅皮层中发现网格细胞以来，神经生理学数据和计算模型已表明这些神经元可服务于PI。然而，由于缺乏对网格细胞活性的选择性操纵和适当的行为评估，缺少支持该假设的更直接的经验证据。在这里我们报告说，可以通过从海马后区域去除NMDA谷氨酸受体来实现对小鼠网格细胞活性的选择性破坏，并且破坏网格细胞的发射是PI性能受损的原因。值得注意的是，遗传操纵并不影响内侧内嗅皮层和海马中其他空间选择性细胞的活性。通过直接将网格单元活动链接到PI，